• innate immunity
• complement evasion
• streptococcal inhibitor of complement
• secretory leucocyte protease inhibitor

• 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

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 coded molecules as being innate which therefore includes natural antibodies with germline V regions.¹ Perhaps a more conventional definition is that innate mechanisms are those that are not specifically altered by prior exposure to the same pathogen.

In the first part of this paper some examples of subversion of the complement system will be described. The second half describes some much newer work from our laboratory that takes us into aspects of the innate immune response on mucosal surfaces that have not so far been described.