REPORT

Subversion of the innate immune response by micro-organisms

B Fernie-King, D J Seilly, A Davies, P J Lachmann

Microbial Immunology Group, Centre for Veterinary Science, University of Cambridge, Madingley Road, Cambridge, CB3 0ES, UK

Correspondence to:
Correspondence to:
Professor Sir P L Lachmann;
pjl1000@cam.ac.uk

Keywords: innate immunity; complement evasion; streptococcal inhibitor of complement; secretory leucocyte protease inhibitor

Abbreviations: BSA, bovine serum albumin; CCP, complement control protein; GAS, group A streptococci; HEL, hen egg lysozyme; MAC, membrane attack complex; SCR, short consensus repeat; SIC, streprococcal inhibitor of complement; SLPI, secretory leucocyte protease inhibitor

The first 150 words of the full text of this article appear below.

A microbe becomes a pathogen by successfully evading the host’s immune responses, and the microbial strategies for so doing are legion. They include methods to avoid recognition by the immune system—for example, by antigenic variation as shown by influenza and HIV and by parasites or plasmodia, or by acquiring a host coat as is done by worms and retroviruses.

Another major mechanism is to avoid the effector mechanisms of the immune response. This can be done by subverting cytotoxic T cells by the production of decoy HLA molecules; or by subverting Fc function by producing Fc receptor homologues; or by subverting complement by producing homologues of complement control proteins (CCPs). Some viruses also have developed methods of subverting apoptosis in the cells that they infect.

This paper concentrates on the innate immune response. The definition of this term is a little fuzzy. Fearon and Locksley regard all mechanisms using germline . . . [Full text of this article]

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This article has been cited by other articles:

• Elphick, D A, Mahida, Y R (2005). Paneth cells: their role in innate immunity and inflammatory disease. Gut 54: 1802-1809 [Full Text]