Disguise as an evasive stratagem of parasitic organisms

Abstract

It is now well established that animal parasites elicit vigorous immune responses in their hosts and that the resistance to reinfection thus acquired is mediated through conventional humoral and/or cellular effector mechanisms. It is also recognized, however, that some parasites exhibit extreme longevity in the face of a potentially hostile or lethal environment, and it may be assumed therefore that such organisms possess a repertoire of highly sophisticated and successful evasive strategies. Of all the survival mechanisms thus far proposed, the concept of antigen sharing, or disguise, is probably the most contentious. Arguments have arisen over the nature and origin of the shared determinants and over the validity of their role in ensuring parasite survival within the fully immunocompetent host. This presentation reviews published data concerning the existence of a disguise stratagem amongst medically important parasites and evaluates experiments designed to investigate the functional importance of disguise in immune evasion.

Excretory/Secretory Proteome of the Adult Developmental Stage of Human Blood Fluke, Schistosoma japonicum

“…These dominant evasion strategies have been described as a system of mimicry capable of producing antigens that are similar to endogenous host components (2-4), antigen disguise through acquisition of host molecules to cover the outer worm surface (5,6), and immunological modulation through interference with host immune systems (7)(8)(9)(10). Among these strategies, schistosome excretory/secretory (ES) 1 products have been shown to elicit host immunological modulation functions (7,11).…”

The Complement System

“…The tool that made this goal achievable was furnished by Petersen and Sober in form of cellulose derived ion exchange media. From Levine's data it was suspected that EAC142 decayed to EAC14 but formal experiments had not yet been performed to prove this (14). (By this time Rapp showed that "C3" was composed of at least two factors, (9)).…”

“…Binding to different structural domains on DAF suggests independent, yet repeating, evolution. CAR expression alone in transfected cells is sufficient to permit infection by all CB viruses (14,15). Other enteroviruses that bind DAF, such as Coxsackieviruses A21, B1, B3, B5 and enterovirus 70, also demonstrate independent evolution of binding.…”

“…RSA may be initiated or prevented by the maternal immune system. Fetomaternal tolerance is partially dependent on the secretion of immunoregulatory cytokines, such as and IL-10, by the decidua and placenta (13)(14)(15)(16). Fetal survival during pregnancy depends in significant measure on the ability of fetal tissue to avoid recognition and rejection by the maternal immune system.…”

“…The fetus expresses many paternally-derived cell surface molecules foreign to the immune system of the mother. Conditions associated with recurrent spontaneous miscarriages and preterm labor are associated with an inflammatory reaction, the production of proinflammatory cytokines such as IL-6, IL-1, and and a conversion from a Th2 to a Th1 phenotype (14,17). Evidence from murine and human pregnancy studies points to a strong association between maternal T helper 2-type (Th2-type) immunity and successful pregnancy, whereas Th1type immune reactivity is associated with pregnancy loss (12).…”