Abstract
BALB.xid mice, carrying an X-linked mutation leading to the absence of CD5+ B cells, are highly resistant to Trypanosoma cruzi infection. These mice clear blood parasites in the acute phase of infection and do not develop the inflammatory infiltration characteristically observed in the chronic phase of susceptible strains of mice. We have shown that the resistance of BALB.xid is dependent on the production of high levels of IFN-gamma. Natural (adoptive foster) or artificial (in vivo injection of blocking antibodies) treatments of BALB.xid induced deletion of CD4+ and CD8+ cells bearing V beta 6 TCR. The absence of V beta 6 lymphocytes considerably reduced resistance to infection. Furthermore, in BALB.xid lacking this minor fraction of the T cell repertoire, almost 50% of the IFN-gamma production is lost. This indicates that V beta 6-bearing T cells are either directly or indirectly involved in the production of IFN-gamma and, thus, important for an effective immune response during the acute phase of experimental Chagas' disease.
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