Trypanosoma cruzi antigen immunization induces a higher B cell survival in BALB/c mice, a susceptible strain, compared to C57BL/6 B lymphocytes, a resistant strain to cardiac autoimmunity

MEDICAL MICROBIOLOGY AND IMMUNOLOGY

SPRINGER

Lugar: Berlin; Año: 2010

0300-8584

Abstract: Chagas disease, caused by Trypanosoma cruzi,is endemic in Latin America and represents the mostcommon infectious myocarditis worldwide. Autoimmunityis one of the mechanisms contributing to its pathogenesis.Although the cellular interactions that promote this autoimmuneresponse are still poorly understood, severalstudies have demonstrated a key role for B lymphocytessince they secrete antibodies, cytokines and present antigens.Recently, we reported that immunization with cruzipain,an immunodominant T. cruzi antigen, induces ahigher activation state in B cells from BALB/c mice(susceptible to cardiac autoimmunity) than B lymphocytesfrom C57BL/6 (a resistant strain). Here, we focused on thestudy of B cell survival in both mouse strains after cruzipainimmunization and demonstrated an increased survivalrate of B cells from BALB/c compared to C57BL/6mice. This phenomenon was associated with a decreasedexpression of Fas/FasL and an increased expression of antiapoptoticBcl-2/Bcl-xL proteins. With the purpose to gainmore knowledge about the mechanisms involved, we foundthat IL-4 produced by BALB/c B cells played a key role inthe survival in an autocrine way whereas the addition ofthis bioactive cytokine rescued C57BL/6 B lymphocytesfrom apoptosis. Our findings suggest that in the absence ofinfection, both enhanced B cell activation induced bythe immunization with a single parasite antigen andinsufficient negative regulation can potentially contributeto autoimmunity seen in cruzipain immune BALB/c mice.