Type I interferons in infectious disease (original) (raw)
Pestka, S., Krause, C. D. & Walter, M. R. Interferons, interferon-like cytokines, and their receptors. Immunol. Rev.202, 8–32 (2004). CASPubMed Google Scholar
Schoenborn, J. R. & Wilson, C. B. Regulation of interferon-γ during innate and adaptive immune responses. Adv. Immunol.96, 41–101 (2007). CASPubMed Google Scholar
O'Brien, T. R., Prokunina-Olsson, L. & Donnelly, R. P. IFN-λ4: the paradoxical new member of the interferon λ family. J. Interferon Cytokine Res.34, 829–838 (2014). CASPubMedPubMed Central Google Scholar
Prokunina-Olsson, L. et al. A variant upstream of IFNL3 (IL28B) creating a new interferon gene IFNL4 is associated with impaired clearance of hepatitis C virus. Nature Genet.45, 164–171 (2013). CASPubMed Google Scholar
Witte, K., Witte, E., Sabat, R. & Wolk, K. IL-28A, IL-28B, and IL-29: promising cytokines with type I interferon-like properties. Cytokine Growth Factor Rev.21, 237–251 (2010). CASPubMed Google Scholar
Durbin, R. K., Kotenko, S. V. & Durbin, J. E. Interferon induction and function at the mucosal surface. Immunol. Rev.255, 25–39 (2013). PubMedPubMed Central Google Scholar
Yan, N. & Chen, Z. J. Intrinsic antiviral immunity. Nature Immunol.13, 214–222 (2012). CAS Google Scholar
Goubau, D., Deddouche, S. & Reis e Sousa, C. Cytosolic sensing of viruses. Immunity38, 855–869 (2013). CASPubMed Google Scholar
Leber, J. H. et al. Distinct TLR- and NLR-mediated transcriptional responses to an intracellular pathogen. PLoS Pathog.4, e6 (2008). PubMedPubMed Central Google Scholar
Pandey, A. K. et al. NOD2, RIP2 and IRF5 play a critical role in the type I interferon response to Mycobacterium tuberculosis. PLoS Pathog.5, e1000500 (2009). PubMedPubMed Central Google Scholar
Watanabe, T. et al. NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway. J. Clin. Invest.120, 1645–1662 (2010). CASPubMedPubMed Central Google Scholar
Moreira, L. O. & Zamboni, D. S. NOD1 and NOD2 signaling in infection and inflammation. Front. Immunol.3, 328 (2012). PubMedPubMed Central Google Scholar
Moynagh, P. N. TLR signalling and activation of IRFs: revisiting old friends from the NF-κB pathway. Trends Immunol.26, 469–476 (2005). CASPubMed Google Scholar
Honda, K., Takaoka, A. & Taniguchi, T. Type I interferon gene induction by the interferon regulatory factor family of transcription factors. Immunity25, 349–360 (2006). CASPubMed Google Scholar
Tamura, T., Yanai, H., Savitsky, D. & Taniguchi, T. The IRF family transcription factors in immunity and oncogenesis. Annu. Rev. Immunol.26, 535–584 (2008). CASPubMed Google Scholar
Ivashkiv, L. B. & Donlin, L. T. Regulation of type I interferon responses. Nature Rev. Immunol.14, 36–49 (2014). This review is a perfect prelude to the present review and describes the molecular mechanisms of regulation of type I IFNs in more detail. CAS Google Scholar
Rauch, I., Muller, M. & Decker, T. The regulation of inflammation by interferons and their STATs. JAKSTAT2, e23820 (2013). PubMedPubMed Central Google Scholar
Versteeg, G. A. & Garcia-Sastre, A. Viral tricks to grid-lock the type I interferon system. Curr. Opin. Microbiol.13, 508–516 (2010). CASPubMedPubMed Central Google Scholar
McNab, F. W., Rajsbaum, R., Stoye, J. P. & O'Garra, A. Tripartite-motif proteins and innate immune regulation. Curr. Opin. Immunol.23, 46–56 (2011). CASPubMed Google Scholar
Diamond, M. S. & Schoggins, J. W. Host restriction factor screening: let the virus do the work. Cell Host Microbe14, 229–231 (2013). CASPubMed Google Scholar
Muller, U. et al. Functional role of type I and type II interferons in antiviral defense. Science264, 1918–1921 (1994). CASPubMed Google Scholar
Haller, O., Arnheiter, H., Gresser, I. & Lindenmann, J. Virus-specific interferon action. Protection of newborn Mx carriers against lethal infection with influenza virus. J. Exp. Med.154, 199–203 (1981). CASPubMed Google Scholar
Durbin, J. E. et al. Type I IFN modulates innate and specific antiviral immunity. J. Immunol.164, 4220–4228 (2000). CASPubMed Google Scholar
Garcia-Sastre, A. et al. The role of interferon in influenza virus tissue tropism. J. Virol.72, 8550–8558 (1998). CASPubMedPubMed Central Google Scholar
Koerner, I., Kochs, G., Kalinke, U., Weiss, S. & Staeheli, P. Protective role of β interferon in host defense against influenza A virus. J. Virol.81, 2025–2030 (2007). CASPubMed Google Scholar
Price, G. E., Gaszewska-Mastarlarz, A. & Moskophidis, D. The role of α/β and γ interferons in development of immunity to influenza A virus in mice. J. Virol.74, 3996–4003 (2000). CASPubMedPubMed Central Google Scholar
Mordstein, M. et al. λ Interferon renders epithelial cells of the respiratory and gastrointestinal tracts resistant to viral infections. J. Virol.84, 5670–5677 (2010). CASPubMedPubMed Central Google Scholar
Mordstein, M. et al. Interferon-λ contributes to innate immunity of mice against influenza A virus but not against hepatotropic viruses. PLoS Pathog.4, e1000151 (2008). This study demonstrates the redundant roles of type I and type III IFNs in the anti-influenza virus response, clarifying the confusion arising from earlier literature that reported that type I IFNs cannot account for the requirement for STAT1 signalling in protection against influenza virus infection. PubMedPubMed Central Google Scholar
Crotta, S. et al. Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia. PLoS Pathog.9, e1003773 (2013). This study demonstrates the redundant roles of type I and type III IFN signalling in epithelial cells in the anti-influenza virus response, clarifying the confusion arising from earlier literature over protection against influenza virus infection. PubMedPubMed Central Google Scholar
Casanova, J. L., Holland, S. M. & Notarangelo, L. D. Inborn errors of human JAKs and STATs. Immunity36, 515–528 (2012). CASPubMedPubMed Central Google Scholar
Zhang, S. Y. et al. Inborn errors of interferon (IFN)-mediated immunity in humans: insights into the respective roles of IFN-α/β, IFN-γ, and IFN-λ in host defense. Immunol. Rev.226, 29–40 (2008). CASPubMed Google Scholar
Suppiah, V. et al. IL28B is associated with response to chronic hepatitis C interferon-α and ribavirin therapy. Nature Genet.41, 1100–1104 (2009). CASPubMed Google Scholar
Tanaka, Y. et al. Genome-wide association of IL28B with response to pegylated interferon-α and ribavirin therapy for chronic hepatitis C. Nature Genet.41, 1105–1109 (2009). CASPubMed Google Scholar
Ge, D. et al. Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance. Nature461, 399–401 (2009). CASPubMed Google Scholar
Thomas, D. L. et al. Genetic variation in IL28B and spontaneous clearance of hepatitis C virus. Nature461, 798–801 (2009). CASPubMedPubMed Central Google Scholar
Sandler, N. G. et al. Type I interferon responses in rhesus macaques prevent SIV infection and slow disease progression. Nature511, 601–605 (2014). CASPubMedPubMed Central Google Scholar
Everitt, A. R. et al. IFITM3 restricts the morbidity and mortality associated with influenza. Nature484, 519–523 (2012). This study provided the first evidence of host genetics (IFITM3) contributing to susceptibility to influenza virus infection in humans. CASPubMedPubMed Central Google Scholar
Zhang, Y. H. et al. Interferon-induced transmembrane protein-3 genetic variant rs12252-C is associated with severe influenza in Chinese individuals. Nature Commun.4, 1418 (2013). This is a follow-up study to reference 38, showing thatIFITM3variants that contribute to the severity of influenza virus infection are predominant in the Chinese population. Google Scholar
Staeheli, P., Grob, R., Meier, E., Sutcliffe, J. G. & Haller, O. Influenza virus-susceptible mice carry Mx genes with a large deletion or a nonsense mutation. Mol. Cell. Biol.8, 4518–4523 (1988). CASPubMedPubMed Central Google Scholar
Horisberger, M. A., Staeheli, P. & Haller, O. Interferon induces a unique protein in mouse cells bearing a gene for resistance to influenza virus. Proc. Natl Acad. Sci. USA80, 1910–1914 (1983). CASPubMed Google Scholar
Horby, P., Nguyen, N. Y., Dunstan, S. J. & Baillie, J. K. The role of host genetics in susceptibility to influenza: a systematic review. PLoS ONE7, e33180 (2012). CASPubMedPubMed Central Google Scholar
Dauer, M. et al. Interferon-α disables dendritic cell precursors: dendritic cells derived from interferon-α-treated monocytes are defective in maturation and T-cell stimulation. Immunology110, 38–47 (2003). CASPubMedPubMed Central Google Scholar
Lapenta, C. et al. Potent immune response against HIV-1 and protection from virus challenge in hu-PBL-SCID mice immunized with inactivated virus-pulsed dendritic cells generated in the presence of IFN-α. J. Exp. Med.198, 361–367 (2003). CASPubMedPubMed Central Google Scholar
Santini, S. M. et al. Type I interferon as a powerful adjuvant for monocyte-derived dendritic cell development and activity in vitro and in Hu-PBL-SCID mice. J. Exp. Med.191, 1777–1788 (2000). CASPubMedPubMed Central Google Scholar
Santodonato, L. et al. Monocyte-derived dendritic cells generated after a short-term culture with IFN-α and granulocyte-macrophage colony-stimulating factor stimulate a potent Epstein-Barr virus-specific CD8+ T cell response. J. Immunol.170, 5195–5202 (2003). CASPubMed Google Scholar
Hahm, B., Trifilo, M. J., Zuniga, E. I. & Oldstone, M. B. Viruses evade the immune system through type I interferon-mediated STAT2-dependent, but STAT1-independent, signaling. Immunity22, 247–257 (2005). CASPubMed Google Scholar
Ito, T. et al. Differential regulation of human blood dendritic cell subsets by IFNs. J. Immunol.166, 2961–2969 (2001). CASPubMed Google Scholar
Montoya, M. et al. Type I interferons produced by dendritic cells promote their phenotypic and functional activation. Blood99, 3263–3271 (2002). CASPubMed Google Scholar
Le Bon, A. et al. Cross-priming of CD8+ T cells stimulated by virus-induced type I interferon. Nature Immunol.4, 1009–1015 (2003). CAS Google Scholar
Le Bon, A. et al. Direct stimulation of T cells by type I IFN enhances the CD8+ T cell response during cross-priming. J. Immunol.176, 4682–4689 (2006). CASPubMed Google Scholar
Spadaro, F. et al. IFN-α enhances cross-presentation in human dendritic cells by modulating antigen survival, endocytic routing, and processing. Blood119, 1407–1417 (2012). CASPubMed Google Scholar
Parlato, S. et al. Expression of CCR-7, MIP-3β, and Th-1 chemokines in type I IFN-induced monocyte-derived dendritic cells: importance for the rapid acquisition of potent migratory and functional activities. Blood98, 3022–3029 (2001). CASPubMed Google Scholar
Rouzaut, A. et al. Dendritic cells adhere to and transmigrate across lymphatic endothelium in response to IFN-α. Eur. J. Immunol.40, 3054–3063 (2010). CASPubMed Google Scholar
Gautier, G. et al. A type I interferon autocrine–paracrine loop is involved in Toll-like receptor-induced interleukin-12p70 secretion by dendritic cells. J. Exp. Med.201, 1435–1446 (2005). CASPubMedPubMed Central Google Scholar
Cousens, L. P., Orange, J. S., Su, H. C. & Biron, C. A. Interferon-α/β inhibition of interleukin 12 and interferon-γ production in vitro and endogenously during viral infection. Proc. Natl Acad. Sci. USA94, 634–639 (1997). CASPubMed Google Scholar
Dalod, M. et al. Interferon α/β and interleukin 12 responses to viral infections: pathways regulating dendritic cell cytokine expression in vivo. J. Exp. Med.195, 517–528 (2002). CASPubMedPubMed Central Google Scholar
Orange, J. S., Wolf, S. F. & Biron, C. A. Effects of IL-12 on the response and susceptibility to experimental viral infections. J. Immunol.152, 1253–1264 (1994). CASPubMed Google Scholar
Orange, J. S. et al. Mechanism of interleukin 12-mediated toxicities during experimental viral infections: role of tumor necrosis factor and glucocorticoids. J. Exp. Med.181, 901–914 (1995). CASPubMed Google Scholar
Le Bon, A. et al. Enhancement of antibody responses through direct stimulation of B and T cells by type I IFN. J. Immunol.176, 2074–2078 (2006). CASPubMed Google Scholar
Havenar-Daughton, C., Kolumam, G. A. & Murali-Krishna, K. The direct action of type I IFN on CD4 T cells is critical for sustaining clonal expansion in response to a viral but not a bacterial infection. J. Immunol.176, 3315–3319 (2006). CASPubMed Google Scholar
Brinkmann, V., Geiger, T., Alkan, S. & Heusser, C. H. Interferon α increases the frequency of interferon γ-producing human CD4+ T cells. J. Exp. Med.178, 1655–1663 (1993). CASPubMed Google Scholar
Hofer, M. J. et al. Mice deficient in STAT1 but not STAT2 or IRF9 develop a lethal CD4+ T-cell-mediated disease following infection with lymphocytic choriomeningitis virus. J. Virol.86, 6932–6946 (2012). CASPubMedPubMed Central Google Scholar
Lazear, H. M., Pinto, A. K., Vogt, M. R., Gale, M. Jr & Diamond, M. S. β-Interferon controls West Nile virus infection and pathogenesis in mice. J. Virol.85, 7186–7194 (2011). CASPubMedPubMed Central Google Scholar
Shiow, L. R. et al. CD69 acts downstream of interferon-α/β to inhibit S1P1 and lymphocyte egress from lymphoid organs. Nature440, 540–544 (2006). CASPubMed Google Scholar
Petricoin, E. F. et al. Antiproliferative action of interferon-α requires components of T-cell-receptor signalling. Nature390, 629–632 (1997). CASPubMed Google Scholar
Kaser, A., Nagata, S. & Tilg, H. Interferon α augments activation-induced T cell death by upregulation of Fas (CD95/APO-1) and Fas ligand expression. Cytokine11, 736–743 (1999). CASPubMed Google Scholar
Marshall, H. D., Urban, S. L. & Welsh, R. M. Virus-induced transient immune suppression and the inhibition of T cell proliferation by type I interferon. J. Virol.85, 5929–5939 (2011). CASPubMedPubMed Central Google Scholar
Bromberg, J. F., Horvath, C. M., Wen, Z., Schreiber, R. D. & Darnell, J. E. Jr. Transcriptionally active Stat1 is required for the antiproliferative effects of both interferon α and interferon γ. Proc. Natl. Acad. Sci. USA93, 7673–7678 (1996). CASPubMed Google Scholar
Lee, C. K., Smith, E., Gimeno, R., Gertner, R. & Levy, D. E. STAT1 affects lymphocyte survival and proliferation partially independent of its role downstream of IFN-γ. J. Immunol.164, 1286–1292 (2000). CASPubMed Google Scholar
Tanabe, Y. et al. Role of STAT1, STAT3, and STAT5 in IFN-α/β responses in T lymphocytes. J. Immunol.174, 609–613 (2005). CASPubMed Google Scholar
Marrack, P., Kappler, J. & Mitchell, T. Type I interferons keep activated T cells alive. J. Exp. Med.189, 521–530 (1999). CASPubMedPubMed Central Google Scholar
Aichele, P. et al. CD8 T cells specific for lymphocytic choriomeningitis virus require type I IFN receptor for clonal expansion. J. Immunol.176, 4525–4529 (2006). CASPubMed Google Scholar
Kolumam, G. A., Thomas, S., Thompson, L. J., Sprent, J. & Murali-Krishna, K. Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection. J. Exp. Med.202, 637–650 (2005). CASPubMedPubMed Central Google Scholar
Curtsinger, J. M., Valenzuela, J. O., Agarwal, P., Lins, D. & Mescher, M. F. Type I IFNs provide a third signal to CD8 T cells to stimulate clonal expansion and differentiation. J. Immunol.174, 4465–4469 (2005). CASPubMed Google Scholar
Keppler, S. J., Rosenits, K., Koegl, T., Vucikuja, S. & Aichele, P. Signal 3 cytokines as modulators of primary immune responses during infections: the interplay of type I IFN and IL-12 in CD8 T cell responses. PLoS ONE7, e40865 (2012). CASPubMedPubMed Central Google Scholar
Gimeno, R., Lee, C. K., Schindler, C. & Levy, D. E. Stat1 and Stat2 but not Stat3 arbitrate contradictory growth signals elicited by α/β interferon in T lymphocytes. Mol. Cell. Biol.25, 5456–5465 (2005). CASPubMedPubMed Central Google Scholar
Gil, M. P., Salomon, R., Louten, J. & Biron, C. A. Modulation of STAT1 protein levels: a mechanism shaping CD8 T-cell responses in vivo. Blood107, 987–993 (2006). CASPubMedPubMed Central Google Scholar
Agarwal, P. et al. Gene regulation and chromatin remodeling by IL-12 and type I IFN in programming for CD8 T cell effector function and memory. J. Immunol.183, 1695–1704 (2009). CASPubMedPubMed Central Google Scholar
Marshall, H. D., Prince, A. L., Berg, L. J. & Welsh, R. M. IFN-α/β and self-MHC divert CD8 T cells into a distinct differentiation pathway characterized by rapid acquisition of effector functions. J. Immunol.185, 1419–1428 (2010). CASPubMedPubMed Central Google Scholar
Cousens, L. P. et al. Two roads diverged: interferon α/β- and interleukin 12-mediated pathways in promoting T cell interferon γ responses during viral infection. J. Exp. Med.189, 1315–1328 (1999). CASPubMedPubMed Central Google Scholar
Nguyen, K. B. et al. Critical role for STAT4 activation by type 1 interferons in the interferon-γ response to viral infection. Science297, 2063–2066 (2002). CASPubMed Google Scholar
Nguyen, K. B. et al. Interferon α/β-mediated inhibition and promotion of interferon γ: STAT1 resolves a paradox. Nature Immunol.1, 70–76 (2000). CAS Google Scholar
Thompson, L. J., Kolumam, G. A., Thomas, S. & Murali-Krishna, K. Innate inflammatory signals induced by various pathogens differentially dictate the IFN-I dependence of CD8 T cells for clonal expansion and memory formation. J. Immunol.177, 1746–1754 (2006). CASPubMed Google Scholar
Pinto, A. K. et al. A temporal role of type I interferon signaling in CD8+ T cell maturation during acute West Nile virus infection. PLoS Pathog.7, e1002407 (2011). CASPubMedPubMed Central Google Scholar
Ramos, H. J. et al. Reciprocal responsiveness to interleukin-12 and interferon-α specifies human CD8+ effector versus central memory T-cell fates. Blood113, 5516–5525 (2009). CASPubMedPubMed Central Google Scholar
Kohlmeier, J. E., Cookenham, T., Roberts, A. D., Miller, S. C. & Woodland, D. L. Type I interferons regulate cytolytic activity of memory CD8+ T cells in the lung airways during respiratory virus challenge. Immunity33, 96–105 (2010). CASPubMedPubMed Central Google Scholar
Sung, J. H. et al. Chemokine guidance of central memory T cells is critical for antiviral recall responses in lymph nodes. Cell150, 1249–1263 (2012). CASPubMedPubMed Central Google Scholar
Soudja, S. M., Ruiz, A. L., Marie, J. C. & Lauvau, G. Inflammatory monocytes activate memory CD8+ T and innate NK lymphocytes independent of cognate antigen during microbial pathogen invasion. Immunity37, 549–562 (2012). CASPubMedPubMed Central Google Scholar
Crouse, J. et al. Type I interferons protect T cells against NK cell attack mediated by the activating receptor NCR1. Immunity40, 961–973 (2014). CASPubMed Google Scholar
Xu, H. C. et al. Type I interferon protects antiviral CD8+ T cells from NK cell cytotoxicity. Immunity40, 949–960 (2014). CASPubMed Google Scholar
Hwang, I. et al. Activation mechanisms of natural killer cells during influenza virus infection. PLoS ONE7, e51858 (2012). CASPubMedPubMed Central Google Scholar
Martinez, J., Huang, X. & Yang, Y. Direct action of type I IFN on NK cells is required for their activation in response to vaccinia viral infection in vivo. J. Immunol.180, 1592–1597 (2008). CASPubMed Google Scholar
Nguyen, K. B. et al. Coordinated and distinct roles for IFN-α/β, IL-12, and IL-15 regulation of NK cell responses to viral infection. J. Immunol.169, 4279–4287 (2002). CASPubMed Google Scholar
Lucas, M., Schachterle, W., Oberle, K., Aichele, P. & Diefenbach, A. Dendritic cells prime natural killer cells by _trans_-presenting interleukin 15. Immunity26, 503–517 (2007). CASPubMedPubMed Central Google Scholar
Sun, J. C., Ma, A. & Lanier, L. L. IL-15-independent NK cell response to mouse cytomegalovirus infection. J. Immunol.183, 2911–2914 (2009). CASPubMedPubMed Central Google Scholar
Baranek, T. et al. Differential responses of immune cells to type I interferon contribute to host resistance to viral infection. Cell Host Microbe12, 571–584 (2012). CASPubMed Google Scholar
Miyagi, T. et al. High basal STAT4 balanced by STAT1 induction to control type 1 interferon effects in natural killer cells. J. Exp. Med.204, 2383–2396 (2007). CASPubMedPubMed Central Google Scholar
Mack, E. A., Kallal, L. E., Demers, D. A. & Biron, C. A. Type 1 interferon induction of natural killer cell γ interferon production for defense during lymphocytic choriomeningitis virus infection. MBio2, e00169-11 (2011). PubMedPubMed Central Google Scholar
Wang, J., Lin, Q., Langston, H. & Cooper, M. D. Resident bone marrow macrophages produce type 1 interferons that can selectively inhibit interleukin-7-driven growth of B lineage cells. Immunity3, 475–484 (1995). CASPubMed Google Scholar
Lin, Q., Dong, C. & Cooper, M. D. Impairment of T and B cell development by treatment with a type I interferon. J. Exp. Med.187, 79–87 (1998). CASPubMedPubMed Central Google Scholar
Bosio, E., Cluning, C. L. & Beilharz, M. W. Low-dose orally administered type I interferon reduces splenic B cell numbers in mice. J. Interferon Cytokine Res.21, 721–728 (2001). CASPubMed Google Scholar
Le Bon, A. et al. Type I interferons potently enhance humoral immunity and can promote isotype switching by stimulating dendritic cells in vivo. Immunity14, 461–470 (2001). CASPubMed Google Scholar
Swanson, C. L. et al. Type I IFN enhances follicular B cell contribution to the T cell-independent antibody response. J. Exp. Med.207, 1485–1500 (2010). CASPubMedPubMed Central Google Scholar
Coro, E. S., Chang, W. L. & Baumgarth, N. Type I IFN receptor signals directly stimulate local B cells early following influenza virus infection. J. Immunol.176, 4343–4351 (2006). CASPubMed Google Scholar
Chang, W. L. et al. Influenza virus infection causes global respiratory tract B cell response modulation via innate immune signals. J. Immunol.178, 1457–1467 (2007). CASPubMed Google Scholar
Rau, F. C., Dieter, J., Luo, Z., Priest, S. O. & Baumgarth, N. B7-1/2 (CD80/CD86) direct signaling to B cells enhances IgG secretion. J. Immunol.183, 7661–7671 (2009). CASPubMedPubMed Central Google Scholar
Heer, A. K. et al. TLR signaling fine-tunes anti-influenza B cell responses without regulating effector T cell responses. J. Immunol.178, 2182–2191 (2007). CASPubMed Google Scholar
Fink, K. et al. Early type I interferon-mediated signals on B cells specifically enhance antiviral humoral responses. Eur. J. Immunol.36, 2094–2105 (2006). CASPubMed Google Scholar
Bach, P. et al. Vesicular stomatitis virus glycoprotein displaying retrovirus-like particles induce a type I IFN receptor-dependent switch to neutralizing IgG antibodies. J. Immunol.178, 5839–5847 (2007). CASPubMed Google Scholar
Purtha, W. E., Chachu, K. A., Virgin, H. W. & Diamond, M. S. Early B-cell activation after West Nile virus infection requires α/β interferon but not antigen receptor signaling. J. Virol.82, 10964–10974 (2008). CASPubMedPubMed Central Google Scholar
Moseman, E. A. et al. B cell maintenance of subcapsular sinus macrophages protects against a fatal viral infection independent of adaptive immunity. Immunity36, 415–426 (2012). CASPubMedPubMed Central Google Scholar
Biron, C. A. Interferons α and β as immune regulators — a new look. Immunity14, 661–664 (2001). CASPubMed Google Scholar
Davidson, S., Crotta, S., McCabe, T. M. & Wack, A. Pathogenic potential of interferon αβ in acute influenza infection. Nature Commun.5, 3864 (2014). This seminal publication shows that, in contrast to the dogma, type I IFNs can cause morbidity and mortality, as opposed to protection, during influenza virus infection. CAS Google Scholar
Mandl, J. N. et al. Divergent TLR7 and TLR9 signaling and type I interferon production distinguish pathogenic and nonpathogenic AIDS virus infections. Nature Med.14, 1077–1087 (2008). CASPubMed Google Scholar
Jacquelin, B. et al. Nonpathogenic SIV infection of African green monkeys induces a strong but rapidly controlled type I IFN response. J. Clin. Invest.119, 3544–3555 (2009). CASPubMedPubMed Central Google Scholar
Rotger, M. et al. Comparative transcriptomics of extreme phenotypes of human HIV-1 infection and SIV infection in sooty mangabey and rhesus macaque. J. Clin. Invest.121, 2391–2400 (2011). CASPubMedPubMed Central Google Scholar
McNally, J. M. et al. Attrition of bystander CD8 T cells during virus-induced T-cell and interferon responses. J. Virol.75, 5965–5976 (2001). CASPubMedPubMed Central Google Scholar
Chi, B. et al. α and λ interferon together mediate suppression of CD4 T cells induced by respiratory syncytial virus. J. Virol.80, 5032–5040 (2006). CASPubMedPubMed Central Google Scholar
Gil, M. P. et al. Regulating type 1 IFN effects in CD8 T cells during viral infections: changing STAT4 and STAT1 expression for function. Blood120, 3718–3728 (2012). CASPubMedPubMed Central Google Scholar
Herbeuval, J. P. et al. Differential expression of IFN-α and TRAIL/DR5 in lymphoid tissue of progressor versus nonprogressor HIV-1-infected patients. Proc. Natl Acad. Sci. USA103, 7000–7005 (2006). CASPubMed Google Scholar
Hardy, A. W., Graham, D. R., Shearer, G. M. & Herbeuval, J. P. HIV turns plasmacytoid dendritic cells (pDC) into TRAIL-expressing killer pDC and down-regulates HIV coreceptors by Toll-like receptor 7-induced IFN-α. Proc. Natl Acad. Sci. USA104, 17453–17458 (2007). CASPubMed Google Scholar
Herbeuval, J. P. et al. CD4+ T-cell death induced by infectious and noninfectious HIV-1: role of type 1 interferon-dependent, TRAIL/DR5-mediated apoptosis. Blood106, 3524–3531 (2005). CASPubMedPubMed Central Google Scholar
van Grevenynghe, J. et al. Loss of memory B cells during chronic HIV infection is driven by Foxo3a- and TRAIL-mediated apoptosis. J. Clin. Invest.121, 3877–3888 (2011). CASPubMedPubMed Central Google Scholar
Liedtke, C., Groger, N., Manns, M. P. & Trautwein, C. Interferon-α enhances TRAIL-mediated apoptosis by up-regulating caspase-8 transcription in human hepatoma cells. J. Hepatol.44, 342–349 (2006). CASPubMed Google Scholar
Shigeno, M. et al. Interferon-α sensitizes human hepatoma cells to TRAIL-induced apoptosis through DR5 upregulation and NF-κB inactivation. Oncogene22, 1653–1662 (2003). CASPubMed Google Scholar
Toomey, N. L. et al. Induction of a TRAIL-mediated suicide program by interferon α in primary effusion lymphoma. Oncogene20, 7029–7040 (2001). CASPubMed Google Scholar
Teijaro, J. R. et al. Persistent LCMV infection is controlled by blockade of type I interferon signaling. Science340, 207–211 (2013). CASPubMedPubMed Central Google Scholar
Wilson, E. B. et al. Blockade of chronic type I interferon signaling to control persistent LCMV infection. Science340, 202–207 (2013). References 128 and 129 were the first to show that type I IFNs contribute to pathogenesis by inducing suppressive mechanisms in chronic LCMV infection. CASPubMedPubMed Central Google Scholar
Herold, S. et al. Lung epithelial apoptosis in influenza virus pneumonia: the role of macrophage-expressed TNF-related apoptosis-inducing ligand. J. Exp. Med.205, 3065–3077 (2008). CASPubMedPubMed Central Google Scholar
Hogner, K. et al. Macrophage-expressed IFN-β contributes to apoptotic alveolar epithelial cell injury in severe influenza virus pneumonia. PLoS Pathog.9, e1003188 (2013). PubMedPubMed Central Google Scholar
Chaperot, L. et al. Virus or TLR agonists induce TRAIL-mediated cytotoxic activity of plasmacytoid dendritic cells. J. Immunol.176, 248–255 (2006). CASPubMed Google Scholar
Fujikura, D. et al. Type-I interferon is critical for FasL expression on lung cells to determine the severity of influenza. PLoS ONE8, e55321 (2013). CASPubMedPubMed Central Google Scholar
McNally, B., Ye, F., Willette, M. & Flano, E. Local blockade of epithelial PDL-1 in the airways enhances T cell function and viral clearance during influenza virus infection. J. Virol.87, 12916–12924 (2013). CASPubMedPubMed Central Google Scholar
Brincks, E. L. et al. The magnitude of the T cell response to a clinically significant dose of influenza virus is regulated by TRAIL. J. Immunol.187, 4581–4588 (2011). CASPubMedPubMed Central Google Scholar
MacMicking, J. D. Interferon-inducible effector mechanisms in cell-autonomous immunity. Nature Rev. Immunol.12, 367–382 (2012). CAS Google Scholar
Kazar, J., Gillmore, J. D. & Gordon, F. B. Effect of interferon and interferon inducers on infections with a nonviral intracellular microorganism, Chlamydia trachomatis. Infect. Immun.3, 825–832 (1971). CASPubMedPubMed Central Google Scholar
de la Maza, L. M., Peterson, E. M., Goebel, J. M., Fennie, C. W. & Czarniecki, C. W. Interferon-induced inhibition of Chlamydia trachomatis: dissociation from antiviral and antiproliferative effects. Infect. Immun.47, 719–722 (1985). CASPubMedPubMed Central Google Scholar
Ishihara, T. et al. Inhibition of Chlamydia trachomatis growth by human interferon-α: mechanisms and synergistic effect with interferon-γ and tumor necrosis factor-α. Biomed. Res.26, 179–185 (2005). CASPubMed Google Scholar
Rothfuchs, A. G. et al. IFN-α/β-dependent, IFN-γ secretion by bone marrow-derived macrophages controls an intracellular bacterial infection. J. Immunol.167, 6453–6461 (2001). CASPubMed Google Scholar
Rothfuchs, A. G. et al. STAT1 regulates IFN-αβ- and IFN-γ-dependent control of infection with Chlamydia pneumoniae by nonhemopoietic cells. J. Immunol.176, 6982–6990 (2006). CASPubMed Google Scholar
Qiu, H. et al. Type I IFNs enhance susceptibility to Chlamydia muridarum lung infection by enhancing apoptosis of local macrophages. J. Immunol.181, 2092–2102 (2008). CASPubMed Google Scholar
Opitz, B. et al. Legionella pneumophila induces IFNβ in lung epithelial cells via IPS-1 and IRF3, which also control bacterial replication. J. Biol. Chem.281, 36173–36179 (2006). CASPubMed Google Scholar
Plumlee, C. R. et al. Interferons direct an effective innate response to Legionella pneumophila infection. J. Biol. Chem.284, 30058–30066 (2009). CASPubMedPubMed Central Google Scholar
Schiavoni, G. et al. Type I IFN protects permissive macrophages from Legionella pneumophila infection through an IFN-γ-independent pathway. J. Immunol.173, 1266–1275 (2004). CASPubMed Google Scholar
Gold, J. A. et al. Exogenous γ and α/β interferon rescues human macrophages from cell death induced by Bacillus anthracis. Infect. Immun.72, 1291–1297 (2004). CASPubMedPubMed Central Google Scholar
Bukholm, G., Berdal, B. P., Haug, C. & Degre, M. Mouse fibroblast interferon modifies Salmonella typhimurium infection in infant mice. Infect. Immun.45, 62–66 (1984). CASPubMedPubMed Central Google Scholar
Niesel, D. W., Hess, C. B., Cho, Y. J., Klimpel, K. D. & Klimpel, G. R. Natural and recombinant interferons inhibit epithelial cell invasion by Shigella spp. Infect. Immun.52, 828–833 (1986). CASPubMedPubMed Central Google Scholar
Mancuso, G. et al. Type I IFN signaling is crucial for host resistance against different species of pathogenic bacteria. J. Immunol.178, 3126–3133 (2007). CASPubMed Google Scholar
Parker, D. et al. Streptococcus pneumoniae DNA initiates type I interferon signaling in the respiratory tract. MBio2, e00016-11 (2011). PubMedPubMed Central Google Scholar
Weigent, D. A., Huff, T. L., Peterson, J. W., Stanton, G. J. & Baron, S. Role of interferon in streptococcal infection in the mouse. Microb. Pathog.1, 399–407 (1986). CASPubMed Google Scholar
Kelly-Scumpia, K. M. et al. Type I interferon signaling in hematopoietic cells is required for survival in mouse polymicrobial sepsis by regulating CXCL10. J. Exp. Med.207, 319–326 (2010). CASPubMedPubMed Central Google Scholar
Weighardt, H. et al. Type I IFN modulates host defense and late hyperinflammation in septic peritonitis. J. Immunol.177, 5623–5630 (2006). CASPubMed Google Scholar
Freudenberg, M. A. et al. A murine, IL-12-independent pathway of IFN-γ induction by Gram-negative bacteria based on STAT4 activation by type I IFN and IL-18 signaling. J. Immunol.169, 1665–1668 (2002). CASPubMed Google Scholar
Auerbuch, V., Brockstedt, D. G., Meyer-Morse, N., O'Riordan, M. & Portnoy, D. A. Mice lacking the type I interferon receptor are resistant to Listeria monocytogenes. J. Exp. Med.200, 527–533 (2004). CASPubMedPubMed Central Google Scholar
Carrero, J. A., Calderon, B. & Unanue, E. R. Type I interferon sensitizes lymphocytes to apoptosis and reduces resistance to Listeria infection. J. Exp. Med.200, 535–540 (2004). CASPubMedPubMed Central Google Scholar
O'Connell, R. M. et al. Type I interferon production enhances susceptibility to Listeria monocytogenes infection. J. Exp. Med.200, 437–445 (2004). References 155–157 were the first publications demonstrating an adverse effect of type I IFNs in intracellular infection with the bacteriumL. monocytogenes. CASPubMedPubMed Central Google Scholar
Carrero, J. A., Calderon, B. & Unanue, E. R. Lymphocytes are detrimental during the early innate immune response against Listeria monocytogenes. J. Exp. Med.203, 933–940 (2006). CASPubMedPubMed Central Google Scholar
Stockinger, S. et al. Production of type I IFN sensitizes macrophages to cell death induced by Listeria monocytogenes. J. Immunol.169, 6522–6529 (2002). CASPubMed Google Scholar
Zwaferink, H., Stockinger, S., Hazemi, P., Lemmens-Gruber, R. & Decker, T. IFN-β increases listeriolysin O-induced membrane permeabilization and death of macrophages. J. Immunol.180, 4116–4123 (2008). CASPubMed Google Scholar
Zwaferink, H., Stockinger, S., Reipert, S. & Decker, T. Stimulation of inducible nitric oxide synthase expression by β interferon increases necrotic death of macrophages upon Listeria monocytogenes infection. Infect. Immun.76, 1649–1656 (2008). CASPubMedPubMed Central Google Scholar
Dresing, P., Borkens, S., Kocur, M., Kropp, S. & Scheu, S. A fluorescence reporter model defines “Tip-DCs” as the cellular source of interferon β in murine listeriosis. PLoS ONE5, e15567 (2010). CASPubMedPubMed Central Google Scholar
Stockinger, S. et al. Characterization of the interferon-producing cell in mice infected with Listeria monocytogenes. PLoS Pathog.5, e1000355 (2009). PubMedPubMed Central Google Scholar
Rayamajhi, M., Humann, J., Penheiter, K., Andreasen, K. & Lenz, L. L. Induction of IFN-α/β enables Listeria monocytogenes to suppress macrophage activation by IFN-γ. J. Exp. Med.207, 327–337 (2010). CASPubMedPubMed Central Google Scholar
Kearney, S. J. et al. Type I IFNs downregulate myeloid cell IFN-γ receptor by inducing recruitment of an early growth response 3/NGFI-A binding protein 1 complex that silences ifngr1 transcription. J. Immunol.191, 3384–3392 (2013). CASPubMedPubMed Central Google Scholar
Manca, C. et al. Hypervirulent M. tuberculosis W/Beijing strains upregulate type I IFNs and increase expression of negative regulators of the Jak-Stat pathway. J. Interferon Cytokine Res.25, 694–701 (2005). CASPubMed Google Scholar
Ordway, D. et al. The hypervirulent Mycobacterium tuberculosis strain HN878 induces a potent TH1 response followed by rapid down-regulation. J. Immunol.179, 522–531 (2007). CASPubMed Google Scholar
Stanley, S. A., Johndrow, J. E., Manzanillo, P. & Cox, J. S. The type I IFN response to infection with Mycobacterium tuberculosis requires ESX-1-mediated secretion and contributes to pathogenesis. J. Immunol.178, 3143–3152 (2007). CASPubMed Google Scholar
Manca, C. et al. Virulence of a Mycobacterium tuberculosis clinical isolate in mice is determined by failure to induce Th1 type immunity and is associated with induction of IFN-α/β. Proc. Natl Acad. Sci. USA98, 5752–5757 (2001). This study was the first demonstration of type I IFNs contributing to the exacerbation of tuberculosis in experimental mouse models. CASPubMed Google Scholar
Cooper, A. M., Pearl, J. E., Brooks, J. V., Ehlers, S. & Orme, I. M. Expression of the nitric oxide synthase 2 gene is not essential for early control of Mycobacterium tuberculosis in the murine lung. Infect. Immun.68, 6879–6882 (2000). CASPubMedPubMed Central Google Scholar
Berry, M. P. et al. An interferon-inducible neutrophil-driven blood transcriptional signature in human tuberculosis. Nature466, 973–977 (2010). This study provided the first evidence that type I IFN-mediated signalling is associated with active tuberculosis in humans. CASPubMedPubMed Central Google Scholar
Cliff, J. M. et al. Distinct phases of blood gene expression pattern through tuberculosis treatment reflect modulation of the humoral immune response. J. Infect. Dis.207, 18–29 (2013). CASPubMed Google Scholar
Maertzdorf, J. et al. Human gene expression profiles of susceptibility and resistance in tuberculosis. Genes Immun.12, 15–22 (2011). CASPubMed Google Scholar
Ottenhoff, T. H. et al. Genome-wide expression profiling identifies type 1 interferon response pathways in active tuberculosis. PLoS ONE7, e45839 (2012). CASPubMedPubMed Central Google Scholar
Antonelli, L. R. et al. Intranasal poly-IC treatment exacerbates tuberculosis in mice through the pulmonary recruitment of a pathogen-permissive monocyte/macrophage population. J. Clin. Invest.120, 1674–1682 (2010). CASPubMedPubMed Central Google Scholar
Mayer-Barber, K. D. et al. Innate and adaptive interferons suppress IL-1α and IL-1β production by distinct pulmonary myeloid subsets during Mycobacterium tuberculosis infection. Immunity35, 1023–1034 (2011). CASPubMedPubMed Central Google Scholar
McNab, F. W. et al. TPL-2-ERK1/2 signaling promotes host resistance against intracellular bacterial infection by negative regulation of type I IFN production. J. Immunol.191, 1732–1743 (2013). CASPubMedPubMed Central Google Scholar
Redford, P. S. et al. Influenza A virus impairs control of Mycobacterium tuberculosis coinfection through a type I interferon receptor-dependent pathway. J. Infect. Dis.209, 270–274 (2014). CASPubMed Google Scholar
Mayer-Barber, K. D. et al. Caspase-1 independent IL-1β production is critical for host resistance to Mycobacterium tuberculosis and does not require TLR signaling in vivo. J. Immunol.184, 3326–3330 (2010). CASPubMedPubMed Central Google Scholar
de Paus, R. A. et al. Inhibition of the type I immune responses of human monocytes by IFN-α and IFN-β. Cytokine61, 645–655 (2013). CASPubMed Google Scholar
Novikov, A. et al. Mycobacterium tuberculosis triggers host type I IFN signaling to regulate IL-1β production in human macrophages. J. Immunol.187, 2540–2547 (2011). CASPubMedPubMed Central Google Scholar
McNab, F. W. et al. Type I IFN induces IL-10 production in an IL-27-independent manner and blocks responsiveness to IFN-γ for production of IL-12 and bacterial killing in _Mycobacterium tuberculosis_-infected macrophages. J. Immunol.193, 3600–3612 (2014). This key study demonstrates the mechanisms underlying the adverse effects of type I IFNs in tuberculosis, including blocking of the protective type II IFN action, as well as blocking of IL-12, IL-1 and TNF production, in part through IL-10 induction. CASPubMedPubMed Central Google Scholar
Guarda, G. et al. Type I interferon inhibits interleukin-1 production and inflammasome activation. Immunity34, 213–223 (2011). This was the first study to show inhibition of the inflammasome by type I IFNs. CASPubMed Google Scholar
Mayer-Barber, K. D. et al. Host-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalk. Nature511, 99–103 (2014). This seminal study shows the counter-regulatory function of IL-1 and type I IFNs in controlling the outcome ofM. tuberculosisinfection via eicosanoids. CASPubMedPubMed Central Google Scholar
Xu, X. J., Reichner, J. S., Mastrofrancesco, B., Henry, W. L. Jr & Albina, J. E. Prostaglandin E2 suppresses lipopolysaccharide-stimulated IFN-β production. J. Immunol.180, 2125–2131 (2008). This study provided the first demonstration that prostaglandin E2 suppresses lipopolysaccharide-stimulated IFNβ production. CASPubMed Google Scholar
Coulombe, F. et al. Targeted prostaglandin E2 inhibition enhances antiviral immunity through induction of type I interferon and apoptosis in macrophages. Immunity40, 554–568 (2014). CASPubMed Google Scholar
Teles, R. M. et al. Type I interferon suppresses type II interferon-triggered human anti-mycobacterial responses. Science339, 1448–1453 (2013). In this key study, a mechanism is reported for type I IFN-mediated blocking of the protective role of type II IFN in tuberculosis. CASPubMedPubMed Central Google Scholar
Desvignes, L., Wolf, A. J. & Ernst, J. D. Dynamic roles of type I and type II IFNs in early infection with Mycobacterium tuberculosis. J. Immunol.188, 6205–6215 (2012). This important study shows that type I IFNs contribute to protection againstM. tuberculosiswhen type II IFN-mediated signalling is aberrant. CASPubMedPubMed Central Google Scholar
Bogunovic, D. et al. Mycobacterial disease and impaired IFN-γ immunity in humans with inherited ISG15 deficiency. Science337, 1684–1688 (2012). CASPubMedPubMed Central Google Scholar
Mariotti, S. et al. Mycobacterium tuberculosis diverts α interferon-induced monocyte differentiation from dendritic cells into immunoprivileged macrophage-like host cells. Infect. Immun.72, 4385–4392 (2004). CASPubMedPubMed Central Google Scholar
Fernandes-Alnemri, T. et al. The AIM2 inflammasome is critical for innate immunity to Francisella tularensis. Nature Immunol.11, 385–393 (2010). CAS Google Scholar
Henry, T., Brotcke, A., Weiss, D. S., Thompson, L. J. & Monack, D. M. Type I interferon signaling is required for activation of the inflammasome during Francisella infection. J. Exp. Med.204, 987–994 (2007). CASPubMedPubMed Central Google Scholar
Henry, T. et al. Type I IFN signaling constrains IL-17A/F secretion by γδ T cells during bacterial infections. J. Immunol.184, 3755–3767 (2010). CASPubMedPubMed Central Google Scholar
Shah, S. et al. Mycobacterium tuberculosis but not nonvirulent mycobacteria inhibits IFN-β and AIM2 inflammasome-dependent IL-1β production via its ESX-1 secretion system. J. Immunol.191, 3514–3518 (2013). CASPubMedPubMed Central Google Scholar
Al Moussawi, K. et al. Type I interferon induction is detrimental during infection with the Whipple's disease bacterium, Tropheryma whipplei. PLoS Pathog.6, e1000722 (2010). PubMedPubMed Central Google Scholar
de Almeida, L. A. et al. MyD88 and STING signaling pathways are required for IRF3-mediated IFN-β induction in response to Brucella abortus infection. PLoS ONE6, e23135 (2011). CASPubMedPubMed Central Google Scholar
Patel, A. A., Lee-Lewis, H., Hughes-Hanks, J., Lewis, C. A. & Anderson, D. M. Opposing roles for interferon regulatory factor-3 (IRF-3) and type I interferon signaling during plague. PLoS Pathog.8, e1002817 (2012). CASPubMedPubMed Central Google Scholar
Robinson, N. et al. Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium. Nature Immunol.13, 954–962 (2012). CAS Google Scholar
Rathinam, V. A. et al. TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by Gram-negative bacteria. Cell150, 606–619 (2012). CASPubMedPubMed Central Google Scholar
Broz, P. et al. Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1. Nature490, 288–291 (2012). CASPubMedPubMed Central Google Scholar
Martin, F. J. et al. Staphylococcus aureus activates type I IFN signaling in mice and humans through the Xr repeated sequences of protein A. J. Clin. Invest.119, 1931–1939 (2009). CASPubMedPubMed Central Google Scholar
Diefenbach, A. et al. Type 1 interferon (IFNα/β) and type 2 nitric oxide synthase regulate the innate immune response to a protozoan parasite. Immunity8, 77–87 (1998). CASPubMed Google Scholar
Mattner, J. et al. Regulation of type 2 nitric oxide synthase by type 1 interferons in macrophages infected with Leishmania major. Eur. J. Immunol.30, 2257–2267 (2000). CASPubMed Google Scholar
Mattner, J. et al. Protection against progressive leishmaniasis by IFN-β. J. Immunol.172, 7574–7582 (2004). CASPubMed Google Scholar
Khouri, R. et al. IFN-β impairs superoxide-dependent parasite killing in human macrophages: evidence for a deleterious role of SOD1 in cutaneous leishmaniasis. J. Immunol.182, 2525–2531 (2009). CASPubMed Google Scholar
Xin, L. et al. Type I IFN receptor regulates neutrophil functions and innate immunity to Leishmania parasites. J. Immunol.184, 7047–7056 (2010). CASPubMedPubMed Central Google Scholar
Haque, A. et al. Type I interferons suppress CD4+ T-cell-dependent parasite control during blood-stage Plasmodium infection. Eur. J. Immunol.41, 2688–2698 (2011). CASPubMed Google Scholar
Vigario, A. M. et al. Inhibition of Plasmodium yoelii blood-stage malaria by interferon α through the inhibition of the production of its target cell, the reticulocyte. Blood97, 3966–3971 (2001). CASPubMed Google Scholar
Vigario, A. M. et al. Recombinant human IFN-α inhibits cerebral malaria and reduces parasite burden in mice. J. Immunol.178, 6416–6425 (2007). CASPubMed Google Scholar
Voisine, C., Mastelic, B., Sponaas, A. M. & Langhorne, J. Classical CD11c+ dendritic cells, not plasmacytoid dendritic cells, induce T cell responses to Plasmodium chabaudi malaria. Int. J. Parasitol.40, 711–719 (2010). CASPubMed Google Scholar
Liehl, P. et al. Host-cell sensors for Plasmodium activate innate immunity against liver-stage infection. Nature Med.20, 47–53 (2014). CASPubMed Google Scholar
Costa, V. M. et al. Type I IFNs stimulate nitric oxide production and resistance to Trypanosoma cruzi infection. J. Immunol.177, 3193–3200 (2006). CASPubMed Google Scholar
Koga, R. et al. TLR-dependent induction of IFN-β mediates host defense against Trypanosoma cruzi. J. Immunol.177, 7059–7066 (2006). CASPubMed Google Scholar
Lopez, R., Demick, K. P., Mansfield, J. M. & Paulnock, D. M. Type I IFNs play a role in early resistance, but subsequent susceptibility, to the African trypanosomes. J. Immunol.181, 4908–4917 (2008). CASPubMedPubMed Central Google Scholar
Chessler, A. D., Caradonna, K. L., Da'dara, A. & Burleigh, B. A. Type I interferons increase host susceptibility to Trypanosoma cruzi infection. Infect. Immun.79, 2112–2119 (2011). CASPubMedPubMed Central Google Scholar
Une, C., Andersson, J. & Orn, A. Role of IFN-α/β and IL-12 in the activation of natural killer cells and interferon-γ production during experimental infection with Trypanosoma cruzi. Clin. Exp. Immunol.134, 195–201 (2003). CASPubMedPubMed Central Google Scholar
Biondo, C. et al. IFN-α/β signaling is required for polarization of cytokine responses toward a protective type 1 pattern during experimental cryptococcosis. J. Immunol.181, 566–573 (2008). CASPubMed Google Scholar
Biondo, C. et al. Recognition of yeast nucleic acids triggers a host-protective type I interferon response. Eur. J. Immunol.41, 1969–1979 (2011). CASPubMed Google Scholar
del Fresno, C. et al. Interferon-β production via Dectin-1-Syk-IRF5 signaling in dendritic cells is crucial for immunity to C. albicans. Immunity38, 1176–1186 (2013). CASPubMed Google Scholar
Majer, O. et al. Type I interferons promote fatal immunopathology by regulating inflammatory monocytes and neutrophils during Candida infections. PLoS Pathog.8, e1002811 (2012). CASPubMedPubMed Central Google Scholar
Bourgeois, C. et al. Conventional dendritic cells mount a type I IFN response against Candida spp. requiring novel phagosomal TLR7-mediated IFN-β signaling. J. Immunol.186, 3104–3112 (2011). CASPubMed Google Scholar
Inglis, D. O., Berkes, C. A., Hocking Murray, D. R. & Sil, A. Conidia but not yeast cells of the fungal pathogen Histoplasma capsulatum trigger a type I interferon innate immune response in murine macrophages. Infect. Immun.78, 3871–3882 (2010). CASPubMedPubMed Central Google Scholar
Liu, L. et al. Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis. J. Exp. Med.208, 1635–1648 (2011). CASPubMedPubMed Central Google Scholar
van de Veerdonk, F. L. et al. STAT1 mutations in autosomal dominant chronic mucocutaneous candidiasis. N. Engl. J. Med.365, 54–61 (2011). CASPubMed Google Scholar
Morens, D. M., Taubenberger, J. K. & Fauci, A. S. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness. J. Infect. Dis.198, 962–970 (2008). PubMedPubMed Central Google Scholar
Li, W., Moltedo, B. & Moran, T. M. Type I interferon induction during influenza virus infection increases susceptibility to secondary Streptococcus pneumoniae infection by negative regulation of γδ T cells. J. Virol.86, 12304–12312 (2012). CASPubMedPubMed Central Google Scholar
Nakamura, S., Davis, K. M. & Weiser, J. N. Synergistic stimulation of type I interferons during influenza virus coinfection promotes Streptococcus pneumoniae colonization in mice. J. Clin. Invest.121, 3657–3665 (2011). CASPubMedPubMed Central Google Scholar
Shahangian, A. et al. Type I IFNs mediate development of postinfluenza bacterial pneumonia in mice. J. Clin. Invest.119, 1910–1920 (2009). CASPubMedPubMed Central Google Scholar
Tian, X. et al. Poly I:C enhances susceptibility to secondary pulmonary infections by Gram-positive bacteria. PLoS ONE7, e41879 (2012). CASPubMedPubMed Central Google Scholar
Navarini, A. A. et al. Increased susceptibility to bacterial superinfection as a consequence of innate antiviral responses. Proc. Natl Acad. Sci. USA103, 15535–15539 (2006). CASPubMed Google Scholar
Kim, Y. G. et al. Viral infection augments Nod1/2 signaling to potentiate lethality associated with secondary bacterial infections. Cell Host Microbe9, 496–507 (2011). CASPubMedPubMed Central Google Scholar
Ganal, S. C. et al. Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota. Immunity37, 171–186 (2012). CASPubMed Google Scholar
Abt, M. C. et al. Commensal bacteria calibrate the activation threshold of innate antiviral immunity. Immunity37, 158–170 (2012). CASPubMedPubMed Central Google Scholar
Tschurtschenthaler, M. et al. Type I interferon signalling in the intestinal epithelium affects Paneth cells, microbial ecology and epithelial regeneration. Gut63, 1921–1931 (2014). CASPubMed Google Scholar
Kawashima, T. et al. Double-stranded RNA of intestinal commensal but not pathogenic bacteria triggers production of protective interferon-β. Immunity38, 1187–1197 (2013). This study shows that the microbiota contributes to the initial production of protective type I IFNs. References 235 and 236 collectively demonstrate a novel interplay between the microbiota, type I IFNs and consequent protection against pathogens. CASPubMed Google Scholar
Gough, D. J., Messina, N. L., Clarke, C. J., Johnstone, R. W. & Levy, D. E. Constitutive type I interferon modulates homeostatic balance through tonic signaling. Immunity36, 166–174 (2012). CASPubMedPubMed Central Google Scholar