| First Author | Oakley MS | Year | 2014 |
| Journal | Eur J Immunol | Volume | 44 |
| Issue | 9 | Pages | 2680-91 |
| PubMed ID | 25047384 | Mgi Jnum | J:318248 |
| Mgi Id | MGI:6858914 | Doi | 10.1002/eji.201344437 |
| Citation | Oakley MS, et al. (2014) T-bet modulates the antibody response and immune protection during murine malaria. Eur J Immunol 44(9):2680-91 |
| abstractText | 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-gamma by a diverse repertoire of immune cell subsets and a selective expansion of IFN-gamma-producing T cells. These observations may have implications in malaria vaccine design. |
