T-bet modulates the antibody response and immune protection during murine malaria.

摘要: CD4+ T-cell subtypes govern the synthesis of different Ab isotypes and other immune functions. The influence differentiation programs on isotype switching aspects host immunological networks during malaria infection are currently poorly understood. Here, we used Tbx21−/− mice deficient for T-bet, a regulator Th1 differentiation, to examine effect T cells protection nonlethal murine Plasmodium yoelii 17XNL. We found that exhibited significantly lower parasite burden correlated with elevated levels IgG1, indicating T-bet-dependent may be responsible burden. Absence T-bet was also associated transient but significant loss infection, suggesting suppress malaria-induced apoptosis or induce proliferation T cells. However, produced greater numbers Foxp3+CD25+ regulatory T cells, which contribute early contraction Lastly, unimpaired production IFN-γ by diverse repertoire cell subsets selective expansion IFN-γ-producing These observations have implications in vaccine design.