Romani, L., Bistoni, F. & Puccetti, P. Adaptation of Candida albicans to the host environment: the role of morphogenesis in virulence and survival in mammalian hosts. Curr. Opin. Microbiol.6, 338–343 (2003). ArticlePubMed Google Scholar
Gow, N. A., Brown, A. J. & Odds, F. C. Fungal morphogenesis and host invasion. Curr. Opin. Microbiol.5, 366–371 (2002). ArticleCASPubMed Google Scholar
Saville, S. P., Lazzell, A. L., Monteagudo, C. & Lopez-Ribot, J. L. Engineered control of cell morphology in vivo reveals distinct roles for yeast and filamentous forms of Candida albicans during infection. Eukaryot. Cell2, 1053–1060 (2003). ArticleCASPubMedPubMed Central Google Scholar
Wachtler, B., Wilson, D., Haedicke, K., Dalle, F. & Hube, B. From attachment to damage: defined genes of Candida albicans mediate adhesion, invasion and damage during interaction with oral epithelial cells. PLoS ONE6, e17046 (2011). ArticleCASPubMedPubMed Central Google Scholar
Casadevall, A. & Pirofski, L. A. The damage-response framework of microbial pathogenesis. Nature Rev. Microbiol.1, 17–24 (2003). ArticleCAS Google Scholar
Perlroth, J., Choi, B. & Spellberg, B. Nosocomial fungal infections: epidemiology, diagnosis, and treatment. Med. Mycol.45, 321–346 (2007). ArticlePubMed Google Scholar
Kirkpatrick, C. H. Chronic mucocutaneous candidiasis. J. Am. Acad. Dermatol.31, S14–S17 (1994). ArticleCASPubMed Google Scholar
Sendid, B. et al. Anti-glycan antibodies establish an unexpected link between C. albicans and Crohn disease. Med. Sci.25, 473–481 (2009). Google Scholar
Netea, M. G., Brown, G. D., Kullberg, B. J. & Gow, N. A. An integrated model of the recognition of Candida albicans by the innate immune system. Nature Rev. Microbiol.6, 67–78 (2008). This article is the first to propose an integrated model ofC. albicansimmune recognition. ArticleCAS Google Scholar
Romani, L. Immunity to fungal infections. Nature Rev. Immunol.11, 275–288 (2011). An excellent review on fungal pattern recognition and antifungal host defence. ArticleCAS Google Scholar
Bailey, D. A., Feldmann, P. J., Bovey, M., Gow, N. A. & Brown, A. J. The Candida albicans HYR1 gene, which is activated in response to hyphal development, belongs to a gene family encoding yeast cell wall proteins. J. Bacteriol.178, 5353–5360 (1996). ArticleCASPubMedPubMed Central Google Scholar
Hoyer, L. L., Payne, T. L., Bell, M., Myers, A. M. & Scherer, S. Candida albicans ALS3 and insights into the nature of the ALS gene family. Curr. Genet.33, 451–459 (1998). ArticleCASPubMed Google Scholar
Staab, J. F., Ferrer, C. A. & Sundstrom, P. Developmental expression of a tandemly repeated, proline-and glutamine-rich amino acid motif on hyphal surfaces on Candida albicans. J. Biol. Chem.271, 6298–6305 (1996). ArticleCASPubMed Google Scholar
Walker, L. A. et al. Genome-wide analysis of Candida albicans gene expression patterns during infection of the mammalian kidney. Fungal Genet. Biol.46, 210–219 (2009). ArticleCASPubMedPubMed Central Google Scholar
Swoboda, R. K. et al. Structure and regulation of the HSP90 gene from the pathogenic fungus Candida albicans. Infect. Immun.63, 4506–4514 (1995). CASPubMedPubMed Central Google Scholar
Swoboda, R. K. et al. Glycolytic enzymes of Candida albicans are nonubiquitous immunogens during candidiasis. Infect. Immun.61, 4263–4271 (1993). CASPubMedPubMed Central Google Scholar
Luo, G. et al. Candida albicans Hyr1p confers resistance to neutrophil killing and is a potential vaccine target. J. Infect. Dis.201, 1718–1728 (2010). ArticleCASPubMed Google Scholar
Shibata, N., Suzuki, A., Kobayashi, H. & Okawa, Y. Chemical structure of the cell-wall mannan of Candida albicans serotype A and its difference in yeast and hyphal forms. Biochem. J.404, 365–372 (2007). ArticleCASPubMedPubMed Central Google Scholar
Nather, K. & Munro, C. A. Generating cell surface diversity in Candida albicans and other fungal pathogens. FEMS Microbiol. Lett.285, 137–145 (2008). ArticleCASPubMed Google Scholar
Cabib, E. & Bowers, B. Chitin and yeast budding. Localization of chitin in yeast bud scars. J. Biol. Chem.246, 152–159 (1971). CASPubMed Google Scholar
Mora-Montes, H. M. et al. Recognition and blocking of innate immunity cells by Candida albicans chitin. Infect. Immun.79, 1961–1970 (2011). ArticleCASPubMedPubMed Central Google Scholar
Gantner, B. N., Simmons, R. M. & Underhill, D. M. Dectin-1 mediates macrophage recognition of Candida albicans yeast but not filaments. EMBO J.24, 1277–1286 (2005). ArticleCASPubMedPubMed Central Google Scholar
Zheng, X. & Wang, Y. Hgc1, a novel hypha-specific G1 cyclin-related protein regulates Candida albicans hyphal morphogenesis. EMBO J.23, 1845–1856 (2004). ArticleCASPubMedPubMed Central Google Scholar
Xu, X. L. et al. Bacterial peptidoglycan triggers Candida albicans hyphal growth by directly activating the adenylyl cyclase Cyr1p. Cell Host Microbe4, 28–39 (2008). ArticleCASPubMed Google Scholar
Hall, R. A. et al. CO2 acts as a signalling molecule in populations of the fungal pathogen Candida albicans. PLoS Pathog.6, e1001193 (2010). ArticleCASPubMedPubMed Central Google Scholar
Feng, Q., Summers, E., Guo, B. & Fink, G. Ras signaling is required for serum-induced hyphal differentiation in Candida albicans. J. Bacteriol.181, 6339–6346 (1999). CASPubMedPubMed Central Google Scholar
Hudson, D. A. et al. Identification of the dialysable serum inducer of germ-tube formation in Candida albicans. Microbiology150, 3041–3049 (2004). ArticleCASPubMed Google Scholar
Maidan, M. M. et al. The G protein-coupled receptor Gpr1 and the Gα protein Gpa2 act through the cAMP-protein kinase A pathway to induce morphogenesis in Candida albicans. Mol. Biol. Cell16, 1971–1986 (2005). ArticleCASPubMedPubMed Central Google Scholar
Shapiro, R. S. et al. Hsp90 orchestrates temperature-dependent Candida albicans morphogenesis via Ras1-PKA signaling. Curr. Biol.19, 621–629 (2009). ArticleCASPubMedPubMed Central Google Scholar
Deveau, A., Piispanen, A. E., Jackson, A. A. & Hogan, D. A. Farnesol induces hydrogen peroxide resistance in Candida albicans yeast by inhibiting the Ras-cyclic AMP signaling pathway. Eukaryot. Cell9, 569–577 (2010). ArticleCASPubMedPubMed Central Google Scholar
Bockmuhl, D. P. & Ernst, J. F. A potential phosphorylation site for an A-type kinase in the Efg1 regulator protein contributes to hyphal morphogenesis of Candida albicans. Genetics157, 1523–1530 (2001). CASPubMedPubMed Central Google Scholar
Sohn, K., Urban, C., Brunner, H. & Rupp, S. EFG1 is a major regulator of cell wall dynamics in Candida albicans as revealed by DNA microarrays. Mol. Microbiol.47, 89–102 (2003). ArticleCASPubMed Google Scholar
Sinha, I. et al. Cyclin-dependent kinases control septin phosphorylation in Candida albicans hyphal development. Dev. Cell13, 421–432 (2007). ArticleCASPubMed Google Scholar
Bishop, A. et al. Hyphal growth in Candida albicans requires the phosphorylation of Sec2 by the Cdc28-Ccn1/Hgc1 kinase. EMBO J.29, 2930–2942 (2010). ArticleCASPubMedPubMed Central Google Scholar
Chen, J., Lane, S. & Liu, H. A conserved mitogen-activated protein kinase pathway is required for mating in Candida albicans. Mol. Microbiol.46, 1335–1344 (2002). ArticleCASPubMed Google Scholar
Eisman, B. et al. The Cek1 and Hog1 mitogen-activated protein kinases play complementary roles in cell wall biogenesis and chlamydospore formation in the fungal pathogen Candida albicans. Eukaryot. Cell5, 347–358 (2006). ArticleCASPubMedPubMed Central Google Scholar
Baek, Y. U., Martin, S. J. & Davis, D. A. Evidence for novel pH-dependent regulation of Candida albicans Rim101, a direct transcriptional repressor of the cell wall β-glycosidase Phr2. Eukaryot. Cell5, 1550–1559 (2006). ArticleCASPubMedPubMed Central Google Scholar
Lotz, H., Sohn, K., Brunner, H., Muhlschlegel, F. A. & Rupp, S. RBR1, a novel pH-regulated cell wall gene of Candida albicans, is repressed by RIM101 and activated by NRG1. Eukaryot. Cell3, 776–784 (2004). ArticleCASPubMedPubMed Central Google Scholar
Stichternoth, C. et al. Sch9 kinase integrates hypoxia and CO2 sensing to suppress hyphal morphogenesis in Candida albicans. Eukaryot. Cell10, 502–511 (2011). ArticleCASPubMedPubMed Central Google Scholar
Stichternoth, C. & Ernst, J. F. Hypoxic adaptation by Efg1 regulates biofilm formation by Candida albicans. Appl. Environ. Microbiol.75, 3663–3672 (2009). ArticleCASPubMedPubMed Central Google Scholar
Shi, Q. M., Wang, Y. M., Zheng, X. D., Lee, R. T. & Wang, Y. Critical role of DNA checkpoints in mediating genotoxic-stress-induced filamentous growth in Candida albicans. Mol. Biol. Cell18, 815–826 (2007). ArticleCASPubMedPubMed Central Google Scholar
Bachewich, C., Thomas, D. Y. & Whiteway, M. Depletion of a polo-like kinase in Candida albicans activates cyclase-dependent hyphal-like growth. Mol. Biol. Cell14, 2163–2180 (2003). ArticleCASPubMedPubMed Central Google Scholar
Leng, P., Sudbery, P. E. & Brown, A. J. Rad6p represses yeast-hypha morphogenesis in the human fungal pathogen Candida albicans. Mol. Microbiol.35, 1264–1275 (2000). ArticleCASPubMed Google Scholar
da Silva Dantas, A. et al. Thioredoxin regulates multiple hydrogen peroxide-induced signaling pathways in Candida albicans. Mol. Cell. Biol.30, 4550–4563 (2010). ArticleCASPubMedPubMed Central Google Scholar
Beutler, B. Microbe sensing, positive feedback loops, and the pathogenesis of inflammatory diseases. Immunol. Rev.227, 248–263 (2009). ArticleCASPubMedPubMed Central Google Scholar
Ishii, K. J., Koyama, S., Nakagawa, A., Coban, C. & Akira, S. Host innate immune receptors and beyond: making sense of microbial infections. Cell Host Microbe3, 352–363 (2008). ArticleCASPubMed Google Scholar
van de Veerdonk, F. L., Kullberg, B. J., van der Meer, J. W., Gow, N. A. & Netea, M. G. Host–microbe interactions: innate pattern recognition of fungal pathogens. Curr. Opin. Microbiol.11, 305–312 (2008). ArticleCASPubMed Google Scholar
Wheeler, R. T., Kombe, D., Agarwala, S. D. & Fink, G. R. Dynamic, morphotype-specific Candida albicans β-glucan exposure during infection and drug treatment. PLoS Pathog.4, e1000227 (2008). ArticleCASPubMedPubMed Central Google Scholar
Ozinsky, A. et al. The repertoire for pattern recognition of pathogens by the innate immune system is defined by cooperation between Toll-like receptors. Proc. Natl Acad. Sci. USA97, 13766–13771 (2000). ArticleCASPubMedPubMed Central Google Scholar
Bellocchio, S. et al. The contribution of Toll-like/IL-1 receptor superfamily to innate and adaptive immunity to fungal pathogens in vivo. J. Immunol.172, 3059–3069 (2004). ArticleCASPubMed Google Scholar
Murciano, C., Yanez, A., Gil, M. L. & Gozalbo, D. Both viable and killed Candida albicans cells induce in vitro production of TNF-α and IFN-γ in murine cells through a TLR2-dependent signalling. Eur. Cytokine Netw.18, 38–43 (2007). CASPubMed Google Scholar
Netea, M. G. et al. The role of toll-like receptor (TLR) 2 and TLR4 in the host defense against disseminated candidiasis. J. Infect. Dis.185, 1483–1489 (2002). ArticleCASPubMed Google Scholar
van de Veerdonk, F. L. et al. Redundant role of TLR9 for anti-Candida host defense. Immunobiology213, 613–620 (2008). ArticleCASPubMed Google Scholar
Gasparoto, T. H. et al. Absence of functional TLR4 impairs response of macrophages after Candida albicans infection. Med. Mycol.48, 1009–1017 (2010). ArticleCASPubMed Google Scholar
Netea, M. G., van de Veerdonk, F., Verschueren, I., van der Meer, J. W. & Kullberg, B. J. Role of TLR1 and TLR6 in the host defense against disseminated candidiasis. FEMS Immunol. Med. Microbiol.52, 118–123 (2008). ArticleCASPubMed Google Scholar
Brown, G. D. Dectin-1: a signalling non-TLR pattern-recognition receptor. Nature Rev. Immunol.6, 33–43 (2006). ArticleCAS Google Scholar
Rogers, N. C. et al. Syk-dependent cytokine induction by Dectin-1 reveals a novel pattern recognition pathway for C type lectins. Immunity22, 507–517 (2005). ArticleCASPubMed Google Scholar
Gringhuis, S. I. et al. Dectin-1 directs T helper cell differentiation by controlling noncanonical NF-κB activation through Raf-1 and Syk. Nature Immunol.10, 203–213 (2009). ArticleCAS Google Scholar
Gantner, B. N., Simmons, R. M., Canavera, S. J., Akira, S. & Underhill, D. M. Collaborative induction of inflammatory responses by dectin-1 and Toll-like receptor 2. J. Exp. Med.197, 1107–1117 (2003). ArticleCASPubMedPubMed Central Google Scholar
Taylor, P. R. et al. Dectin-1 is required for β-glucan recognition and control of fungal infection. Nature Immunol.8, 31–38 (2007). ArticleCAS Google Scholar
Saijo, S. et al. Dectin-1 is required for host defense against Pneumocystis carinii but not against Candida albicans. Nature Immunol.8, 39–46 (2007). ArticleCAS Google Scholar
Gross, O. et al. Card9 controls a non-TLR signalling pathway for innate anti-fungal immunity. Nature442, 651–656 (2006). ArticleCASPubMed Google Scholar
Glocker, E. O. et al. A homozygous CARD9 mutation in a family with susceptibility to fungal infections. N. Engl. J. Med.361, 1727–1735 (2009). ArticleCASPubMedPubMed Central Google Scholar
Stahl, P. D. & Ezekowitz, R. A. The mannose receptor is a pattern recognition receptor involved in host defense. Curr. Opin. Immunol.10, 50–55 (1998). ArticleCASPubMed Google Scholar
Netea, M. G. et al. Immune sensing of Candida albicans requires cooperative recognition of mannans and glucans by lectin and Toll-like receptors. J. Clin. Invest.116, 1642–1650 (2006). ArticleCASPubMedPubMed Central Google Scholar
Le Cabec, V., Emorine, L. J., Toesca, I., Cougoule, C. & Maridonneau-Parini, I. The human macrophage mannose receptor is not a professional phagocytic receptor. J. Leukoc. Biol.77, 934–943 (2005). ArticleCASPubMed Google Scholar
Heinsbroek, S. E. et al. Stage-specific sampling by pattern recognition receptors during Candida albicans phagocytosis. PLoS Pathog.4, e1000218 (2008). ArticleCASPubMedPubMed Central Google Scholar
van de Veerdonk, F. L. et al. The macrophage mannose receptor induces IL-17 in response to Candida albicans. Cell Host Microbe5, 329–340 (2009). This study is the first to demonstrate the importance of mannose-containing structures in driving TH17 cell responses. ArticleCASPubMed Google Scholar
Ariizumi, K. et al. Cloning of a second dendritic cell-associated C-type lectin (dectin-2) and its alternatively spliced isoforms. J. Biol. Chem.275, 11957–11963 (2000). ArticleCASPubMed Google Scholar
McGreal, E. P. et al. The carbohydrate-recognition domain of Dectin-2 is a C-type lectin with specificity for high mannose. Glycobiology16, 422–430 (2006). ArticleCASPubMed Google Scholar
Sato, K. et al. Dectin-2 is a pattern recognition receptor for fungi that couples with the Fc receptor γ chain to induce innate immune responses. J. Biol. Chem.281, 38854–38866 (2006). ArticleCASPubMed Google Scholar
Robinson, M. J. et al. Dectin-2 is a Syk-coupled pattern recognition receptor crucial for Th17 responses to fungal infection. J. Exp. Med.206, 2037–2051 (2009). ArticleCASPubMedPubMed Central Google Scholar
Koppel, E. A., van Gisbergen, K. P., Geijtenbeek, T. B. & van Kooyk, Y. Distinct functions of DC-SIGN and its homologues L-SIGN (DC-SIGNR) and mSIGNR1 in pathogen recognition and immune regulation. Cell. Microbiol.7, 157–165 (2005). ArticleCASPubMed Google Scholar
Cambi, A. et al. The C-type lectin DC-SIGN (CD209) is an antigen-uptake receptor for Candida albicans on dendritic cells. Eur. J. Immunol.33, 532–538 (2003). ArticleCASPubMed Google Scholar
Cambi, A. et al. Dendritic cell interaction with Candida albicans critically depends on _N_-linked mannan. J. Biol. Chem.283, 20590–20599 (2008). ArticleCASPubMedPubMed Central Google Scholar
Wells, C. A. et al. The macrophage-inducible C-type lectin, Mincle, is an essential component of the innate immune response to Candida albicans. J. Immunol.180, 7404–7413 (2008). ArticleCASPubMed Google Scholar
Means, T. K. et al. Evolutionarily conserved recognition and innate immunity to fungal pathogens by the scavenger receptors SCARF1 and CD36. J. Exp. Med.206, 637–653 (2009). ArticleCASPubMedPubMed Central Google Scholar
Jouault, T. et al. Specific recognition of Candida albicans by macrophages requires galectin-3 to discriminate Saccharomyces cerevisiae and needs association with TLR2 for signaling. J. Immunol.177, 4679–4687 (2006). ArticleCASPubMed Google Scholar
Jawhara, S. et al. Colonization of mice by Candida albicans is promoted by chemically induced colitis and augments inflammatory responses through galectin-3. J. Infect. Dis.197, 972–980 (2008). ArticleCASPubMed Google Scholar
Martinon, F. & Tschopp, J. Inflammatory caspases: linking an intracellular innate immune system to autoinflammatory diseases. Cell117, 561–574 (2004). ArticleCASPubMed Google Scholar
van der Graaf, C. A. et al. Nucleotide oligomerization domain 2 (Nod2) is not involved in the pattern recognition of Candida albicans. Clin. Vaccine Immunol.13, 423–425 (2006). ArticleCASPubMedPubMed Central Google Scholar
Vonk, A. G. et al. Endogenous interleukin (IL)–1α and IL-1β are crucial for host defense against disseminated candidiasis. J. Infect. Dis.193, 1419–1426 (2006). ArticleCASPubMed Google Scholar
Gross, O. et al. Syk kinase signalling couples to the Nlrp3 inflammasome for anti-fungal host defence. Nature459, 433–436 (2009). ArticleCASPubMed Google Scholar
Kumar, H. et al. Involvement of the NLRP3 inflammasome in innate and humoral adaptive immune responses to fungal β-glucan. J. Immunol.183, 8061–8067 (2009). This study finds that there is differential activation of the inflammasome byC. albicansyeast cells and hyphae. ArticleCASPubMed Google Scholar
van de Veerdonk, F. L. et al. The inflammasome drives protective Th1 and Th17 cellular responses in disseminated candidiasis. Eur. J. Immunol.41, 2260–2268 (2011). This investigation demonstrates the importance of the inflammasome in driving protective TH1-type and TH17-type responses during fungal infection. ArticleCASPubMedPubMed Central Google Scholar
Hise, A. G. et al. An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen Candida albicans. Cell Host Microbe5, 487–497 (2009). ArticleCASPubMedPubMed Central Google Scholar
d'Ostiani, C. F. et al. Dendritic cells discriminate between yeasts and hyphae of the fungus Candida albicans. Implications for initiation of T helper cell immunity in vitro and in vivo. J. Exp. Med.191, 1661–1674 (2000). ArticleCASPubMedPubMed Central Google Scholar
van der Graaf, C. A., Netea, M. G., Verschueren, I., van der Meer, J. W. & Kullberg, B. J. Differential cytokine production and Toll-like receptor signaling pathways by Candida albicans blastoconidia and hyphae. Infect. Immun.73, 7458–7464 (2005). ArticleCASPubMedPubMed Central Google Scholar
Cheng, S. C. et al. The dectin-1/inflammasome pathway is responsible for the induction of protective T-helper 17 responses that discriminate between yeasts and hyphae of Candida albicans. J. Leukoc. Biol.90, 357–366 (2011). This article describes the inflammasome–IL-1β–TH17 cell axis as an important mechanism that is capable of discriminatingC. albicanscolonization from invasion at the mucosal level. ArticleCASPubMedPubMed Central Google Scholar
Bi, L. et al. CARD9 mediates dectin-2-induced IκBα kinase ubiquitination leading to activation of NF-κB in response to stimulation by the hyphal form of Candida albicans. J. Biol. Chem.285, 25969–25977 (2010). ArticleCASPubMedPubMed Central Google Scholar
Kruppa, M., Greene, R. R., Noss, I., Lowman, D. W. & Williams, D. L. C. albicans increases cell wall mannoprotein, but not mannan, in response to blood, serum and cultivation at physiological temperature. Glycobiology21, 1173–1180 (2011). ArticleCASPubMedPubMed Central Google Scholar
Scherwitz, C. Ultrastructure of human cutaneous candidosis. J. Invest. Dermatol.78, 200–205 (1982). ArticleCASPubMed Google Scholar
Ray, T. L. & Payne, C. D. Scanning electron microscopy of epidermal adherence and cavitation in murine candidiasis: a role for Candida acid proteinase. Infect. Immun.56, 1942–1949 (1988). CASPubMedPubMed Central Google Scholar
Kumamoto, C. A. & Vinces, M. D. Alternative Candida albicans lifestyles: growth on surfaces. Annu. Rev. Microbiol.59, 113–133 (2005). ArticleCASPubMed Google Scholar
Moyes, D. L. et al. A biphasic innate immune MAPK response discriminates between the yeast and hyphal forms of Candida albicans in epithelial cells. Cell Host Microbe8, 225–235 (2010). A seminal study describing the mechanisms through which epithelial cells can discriminate between colonizing yeast cells and invading hyphae. ArticleCASPubMedPubMed Central Google Scholar
Weindl, G. et al. Human epithelial cells establish direct antifungal defense through TLR4-mediated signaling. J. Clin. Invest.117, 3664–3672 (2007). CASPubMedPubMed Central Google Scholar
Moreno-Ruiz, E. et al. Candida albicans internalization by host cells is mediated by a clathrin-dependent mechanism. Cell. Microbiol.11, 1179–1189 (2009). ArticleCASPubMedPubMed Central Google Scholar
Martin, R., Wachtler, B., Schaller, M., Wilson, D. & Hube, B. Host-pathogen interactions and virulence-associated genes during Candida albicans oral infections. Int. J. Med. Microbiol.301, 417–422 (2011). ArticleCASPubMed Google Scholar
Dalle, F. et al. Cellular interactions of Candida albicans with human oral epithelial cells and enterocytes. Cell. Microbiol.12, 248–271 (2010). ArticleCASPubMed Google Scholar
Park, H. et al. Role of the fungal Ras-protein kinase A pathway in governing epithelial cell interactions during oropharyngeal candidiasis. Cell. Microbiol.7, 499–510 (2005). ArticleCASPubMed Google Scholar
Brand, A. et al. An internal polarity landmark is important for externally induced hyphal behaviors in Candida albicans. Eukaryot. Cell7, 712–720 (2008). ArticleCASPubMedPubMed Central Google Scholar
Hube, B. et al. Disruption of each of the secreted aspartyl proteinase genes SAP1, SAP2, and SAP3 of Candida albicans attenuates virulence. Infect. Immun.65, 3529–3538 (1997). CASPubMedPubMed Central Google Scholar
Naglik, J. R., Challacombe, S. J. & Hube, B. Candida albicans secreted aspartyl proteinases in virulence and pathogenesis. Microbiol. Mol. Biol. Rev.67, 400–428 (2003). ArticleCASPubMedPubMed Central Google Scholar
Ibrahim, A. S. et al. Evidence implicating phospholipase as a virulence factor of Candida albicans. Infect. Immun.63, 1993–1998 (1995). CASPubMedPubMed Central Google Scholar
Weindl, G., Wagener, J. & Schaller, M. Interaction of the mucosal barrier with accessory immune cells during fungal infection. Int. J. Med. Microbiol.301, 431–435 (2011). ArticleCASPubMed Google Scholar
Eyerich, K. et al. Patients with chronic mucocutaneous candidiasis exhibit reduced production of Th17-associated cytokines IL-17 and IL-22. J. Invest. Dermatol.128, 2640–2645 (2008). ArticleCASPubMed Google Scholar
Ng, W. F. et al. Impaired TH17 responses in patients with chronic mucocutaneous candidiasis with and without autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy. J. Allergy Clin. Immunol.126, 1006–1015. e4 (2010). ArticleCASPubMed 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). ArticleCASPubMed 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). ArticleCASPubMedPubMed Central Google Scholar
Puel, A. et al. Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I. J. Exp. Med.207, 291–297 (2010). This paper describes the link betweenSTAT3mutations and defective TH17 cell differentiation. ArticleCASPubMedPubMed Central Google Scholar
Kisand, K. et al. Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th17-associated cytokines. J. Exp. Med.207, 299–30 8 (2010). ArticleCASPubMedPubMed Central Google Scholar
Milner, J. D. et al. Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome. Nature452, 773–776 (2008). ArticleCASPubMedPubMed Central Google Scholar
de Beaucoudrey, L. et al. Mutations in STAT3 and IL12RB1 impair the development of human IL-17–producing T cells. J. Exp. Med.205, 1543–1550 (2008). ArticleCASPubMedPubMed Central Google Scholar
van de Veerdonk, F. L. et al. Milder clinical hyperimmunoglobulin E syndrome phenotype is associated with partial interleukin-17 deficiency. Clin. Exp. Immunol.159, 57–64 (2010). ArticleCASPubMedPubMed Central Google Scholar
Plantinga, T. S. et al. Early stop polymorphism in human DECTIN-1 is associated with increased Candida colonization in hematopoietic stem cell transplant recipients. Clin. Infect. Dis.49, 724–732 (2009). ArticleCASPubMed Google Scholar
Fidel, P. L. Jr. History and update on host defense against vaginal candidiasis. Am. J. Reprod. Immunol.57, 2–12 (2007). ArticlePubMed Google Scholar
Yano, J., Lilly, E., Barousse, M. & Fidel, P. L. Jr. Epithelial cell-derived S100 calcium-binding proteins as key mediators in the hallmark acute neutrophil response during Candida vaginitis. Infect. Immun.78, 5126–5137 (2010). ArticleCASPubMedPubMed Central Google Scholar
Acosta-Rodriguez, E. V. et al. Surface phenotype and antigenic specificity of human interleukin 17-producing T helper memory cells. Nature Immunol.8, 639–646 (2007). ArticleCAS Google Scholar
Acosta-Rodriguez, E. V., Napolitani, G., Lanzavecchia, A. & Sallusto, F. Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17-producing human T helper cells. Nature Immunol.8, 942–949 (2007). ArticleCAS Google Scholar
Bettelli, E. et al. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature441, 235–238 (2006). ArticleCASPubMed Google Scholar
McGeachy, M. J. & Cua, D. J. Th17 cell differentiation: the long and winding road. Immunity28, 445–453 (2008). ArticleCASPubMed Google Scholar
Joly, S. et al. Cutting edge: Candida albicans hyphae formation triggers activation of the Nlrp3 inflammasome. J. Immunol.183, 3578–3581 (2009). ArticleCASPubMed Google Scholar
Cheng, S. C. et al. Candida albicans dampens host defense by downregulating IL-17 production. J. Immunol.185, 2450–2457 (2010). ArticleCASPubMed Google Scholar
van de Veerdonk, F. L. et al. Bypassing pathogen-induced inflammasome activation for the regulation of interleukin-1β production by the fungal pathogen Candida albicans. J. Infect. Dis.199, 1087–1096 (2009). ArticleCASPubMed Google Scholar
Ouyang, W., Kolls, J. K. & Zheng, Y. The biological functions of T helper 17 cell effector cytokines in inflammation. Immunity28, 454–467 (2008). ArticleCASPubMedPubMed Central Google Scholar
Eyerich, S. et al. IL-22 and TNF-α represent a key cytokine combination for epidermal integrity during infection with Candida albicans. Eur. J. Immunol.41, 1894–1901 (2011). ArticleCASPubMed Google Scholar
Piccini, A. et al. ATP is released by monocytes stimulated with pathogen-sensing receptor ligands and induces IL-1β and IL-18 secretion in an autocrine way. Proc. Natl Acad. Sci. USA105, 8067–8072 (2008). An important study highlighting the link between the commensal microbial flora and mucosal TH17 cell immune responses. ArticleCASPubMedPubMed Central Google Scholar
Atarashi, K. et al. ATP drives lamina propria TH17 cell differentiation. Nature455, 808–812 (2008). ArticleCASPubMed Google Scholar