Evasion of human innate and acquired immunity by a bacterial homolog of CD11b that inhibits opsonophagocytosis - PubMed (original) (raw)
. 2001 Dec;7(12):1298-305.
doi: 10.1038/nm1201-1298.
F R DeLeo, N P Hoe, M R Graham, S M Mackie, R L Cole, M Liu, H R Hill, D E Low, M J Federle, J R Scott, J M Musser
Affiliations
- PMID: 11726969
- DOI: 10.1038/nm1201-1298
Evasion of human innate and acquired immunity by a bacterial homolog of CD11b that inhibits opsonophagocytosis
B Lei et al. Nat Med. 2001 Dec.
Abstract
Microbial pathogens must evade the human immune system to survive, disseminate and cause disease. By proteome analysis of the bacterium Group A Streptococcus (GAS), we identified a secreted protein with homology to the alpha-subunit of Mac-1, a leukocyte beta2 integrin required for innate immunity to invading microbes. The GAS Mac-1-like protein (Mac) was secreted by most pathogenic strains, produced in log-phase and controlled by the covR-covS two-component gene regulatory system, which also regulates transcription of other GAS virulence factors. Patients with GAS infection had titers of antibody specific to Mac that correlated with the course of disease, demonstrating that Mac was produced in vivo. Mac bound to CD16 (FcgammaRIIIB) on the surface of human polymorphonuclear leukocytes and inhibited opsonophagocytosis and production of reactive oxygen species, which resulted in significantly decreased pathogen killing. Thus, by mimicking a host-cell receptor required for an innate immune response, the GAS Mac protein inhibits professional phagocyte function by a novel strategy that enhances pathogen survival, establishment of infection and dissemination.
Comment in
- Annihilating host defense.
Frank MM. Frank MM. Nat Med. 2001 Dec;7(12):1285-6. doi: 10.1038/nm1201-1285. Nat Med. 2001. PMID: 11726964 No abstract available. - Streptococcus pyogenes and phagocytic killing.
von Pawel-Rammingen U, Johansson BP, Tapper H, Björck L. von Pawel-Rammingen U, et al. Nat Med. 2002 Oct;8(10):1044-5; author reply 1045-6. doi: 10.1038/nm1002-1044. Nat Med. 2002. PMID: 12357219 No abstract available.
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