Host factors in the pathogenesis of arthritis triggered by infectious organisms. Overview

Individual variability in host immune responses to infectious agents is likely influenced by differences in the repertoires of antigenic peptides bound by self-major histocompatibility complex molecules (MHC) and in the repertoires of T-cell receptors expressed in each individual. Moreover, genes regulating the processing of foreign MHC antigens (for example, peptide pump genes and proteosome constituent genes) may also be important in this regard. Infectious organisms may subvert host immune responses through expression of constituents sharing structure homology with host molecules. Such structural mimicry may serve to either promote induction of potentially harmful cross-reactive autoimmune responses or impede effective host responses, thereby favoring persistence of the organism.