Trypanosoma cruzi: Predominance of IgG2a in nonspecific humoral response during experimental Chagas' disease

Modulation of Cardiocyte Functional Activity by Antibodies againstTrypanosoma cruziRibosomal P2 Protein C Terminus

“…Alternatively, the response against the conserved C terminus of TcP2␤ could parallel the intense B-cell polyclonal activation, increasing the level of autoantibodies during T. cruzi infection (7,8). It is noteworthy that the IgG2a isotype was highly represented in the TcP2␤ response in immunized mice, as well as in infected mice, as previously described for nonspecific and parasite-specific humoral responses (27,35). However, in immunized mice, the IgG1 involved in protection is usually the representative isotype (5,9,30,36,37).…”

Induction of antibodies reactive to cardiac myosin and development of heart alterations in cruzipain-immunized mice and their offspring

“…This latter isotype could lead to complement fixation, inflammation and subsequent pathology in the heart tissue. Of note, IgG2a is the main isotype involved in the production of autoantibodies in the chronic stage of T. cruzi experimental infection [28] and in the development of anti-self B cell responses in autoimmune prone mice that lack functional Fas or FasL [29]. Autoreactive B and T cells are already present in normal animals and humans, indicating that factors other than self recognition "per se" are engaged in the development of autoimmune disease.…”

Chagas' Disease Encephalitis: Intense CD8+ Lymphocytic Infiltrate Is Restricted to the Acute Phase, but Is Not Related to the Presence of Trypanosoma cruzi Antigens

“…In this stage, amastigote forms and parasite antigens were detected in neurons, glia, and microglia in both humans and experimental animals (12,13). The involvement of the immune system in the genesis of neural lesions was proposed on the basis of the existence of peripheral lymphocytes and antibodies specific for nervous system components in infected animals (14,15), but a correlation between the presence of parasite antigens and inflammatory infiltrates within the central nervous system (CNS) has not been attempted so far. Moreover, the composition of such infiltrates in terms of lympho-cyte subsets remains unknown and the persistence of inflammation during the chronic phase is a controversial question (16,11).…”