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- Title
T-bet modulates the antibody response and immune protection during murine malaria.
- Authors
Oakley, Miranda S.; Sahu, Bikash R.; Lotspeich‐Cole, Leda; Majam, Victoria; Thao Pham, Phuong; Sengupta Banerjee, Aditi; Kozakai, Yukiko; Morris, Sheldon L.; Kumar, Sanjai
- Abstract
CD4+ T-cell subtypes govern the synthesis of different Ab isotypes and other immune functions. The influence of CD4+ T-cell differentiation programs on isotype switching and other aspects of host immunological networks during malaria infection are currently poorly understood. Here, we used Tbx21−/− mice deficient for T-bet, a regulator of Th1 CD4+ T-cell differentiation, to examine the effect of Th1 CD4+ T cells on the immune protection to nonlethal murine malaria Plasmodium yoelii 17XNL. We found that Tbx21−/− mice exhibited significantly lower parasite burden that correlated with elevated levels of IgG1, indicating that T-bet-dependent Ab isotype switching may be responsible for lower parasite burden. Absence of T-bet was also associated with a transient but significant loss of T cells during the infection, suggesting that T-bet may suppress malaria-induced apoptosis or induce proliferation of T cells. However, Tbx21−/− mice produced greater numbers of Foxp3+CD25+ regulatory CD4+ T cells, which may contribute to the early contraction of T cells. Lastly, Tbx21−/− mice exhibited unimpaired production of IFN-γ by a diverse repertoire of immune cell subsets and a selective expansion of IFN-γ-producing T cells. These observations may have implications in malaria vaccine design.
- Publication
European Journal of Immunology, 2014, Vol 44, Issue 9, p2680
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.201344437