Gonococci cause immunosuppression by engaging a coinhibitory receptor on T lymphocytes

Abstract

Gonococci that bind the coinhibitory receptor CEACAM1 appear to down-regulate the activation and proliferation of CD4⁺ T cells. Such infection-induced immunosuppression helps explain why there is little specific immune response associated with gonococcal disease.

Figure 1. Expression of the bacterial surface protein Opa₅₂ inhibits activation and proliferation of Neisseria-infected CD4⁺ T lymphocytes.

Immunosuppression is mediated by interactions between Opa₅₂ and the CEACAM1 receptor, which allows the ITIM motif on CEACAM1 to bind tyrosine SHP-1 and SHP-2 phosphatases. This alters the delicate balance between costimulatory and coinhibitory signals. Other surface molecules expressed by gonococci will directly or indirectly immunostimulate, rather than immunosuppress, T cell activation. Those other immunoactivation pathways have not yet been investigated for Neisseria-infected T lymphocytes.