Parasite immunology and lymphocyte population dynamics.
We propose that parasites use "antigenic mimicry", the presentation of host-type antigens, not merely as a disguise, but as a means of actively diverting the immune system into an ineffective mode of response that actually protects the parasites. This suggestion is the outcome of analyzing the immune system by the principle of Darwinian selection--among lymphocyte populations differing in their relative growth capacities under particular environmental conditions. In particular, it is proposed that proliferation can be uncoupled from differentiation under certain predictable conditions; and moreover, clones that proliferate for prolonged periods of time without significant maturation into effector cells may gain a selective advantage and reach prominence. This mode of "latent proliferation" is a key to self-non-self discrimination: under physiologic conditions, those T and B cells are selected that react "proliferatively" with certain classes of self-antigens, ensuring tolerance to self. We suggest that parasites which present host-type antigens generate the same kind of dynamic selection among responding lymphocytes. The hypothesis links polyclonal activation and "immunosuppression" to "antigenic mimicry", predicts "concomitant immunity" to the same parasite and suggests a pathway leading to autoimmunity. It is also amenable to testing.
D000818:Animals; D006790:Host-Parasite Interactions; D006801:Humans; D007165:Immunosuppression Therapy; D007896:Leishmaniasis / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology*; D051379:Mice; D010271:Parasites / Q000276:immunology*