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Polyclonal activation

T. cruzi induces in mouse an abundant and long-lasting polyclonal plasma cell response producing mostly nonparasite specific antibodies,154,184 in which B1-B cells would play an important role.185 Several parasite molecules are involved in polyclonal B cell activation (reviewed by Truyens and Carlier3). Polyclonal activation is thought to constitute an immune evasion mechanism by masking/deviating the specific responses, thereby limiting the control of infection. Moreover, it might participate to enlarge the B repertoire to self-antigens, favoring the production of autoreactive Ab participating in the pathology of the chronic infection.

Escape mechanisms of T. cruzi to the immune responses

Lymphocyte immunosuppression and polyclonal B cell activation indubitably facilitate the parasite to establish in its host. However, as said by Tarleton, “failure to completely eliminate the parasites during acute infection might rather reflects the success of T. cruzi in evading host immune responses than results from a suppressed or dysregulated immune response.”133 Indeed, the parasite also makes use of other remarkable evasion strategies to slow down the initiation of the immune response and limit its effector action. Points discussed hereunder do not constitute an exhaustive list of escape mechanisms, summarized in excellent recent reviews.186-188

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