| Literature DB >> 26276869 |
Tuoqi Wu1, Andreas Wieland1, Judong Lee1, J Scott Hale1, Jin-Hwan Han1, Xiaojin Xu1, Rafi Ahmed2.
Abstract
Viral infections induce the differentiation of naive CD4 T cells into two distinct lineages, Th1 cells and T follicular helper (TFH) cells. Two recent studies demonstrated that the microRNA cluster miR-17-92 selectively promotes CD4 TFH responses. However, we show in this study that miR-17-92 expression is required for the clonal expansion of both virus-specific Th1 and TFH cells. Upon viral infection, miR-17-92-deficient CD4 T cells showed impaired clonal expansion and subsequent memory formation. Although miR-17-92 deficiency impaired the clonal expansion of both Th1 and TFH cells, the expansion of Th1 cells was more affected. Overexpression of miR-17-92 in CD4 T cells resulted in increased expansion of both virus-specific Th1 and TFH cells but selectively enhanced the Th1 response. Taken together, our data suggest that miR-17-92 is necessary for both Th1 and TFH cells to respond efficiently to viral infections and that the Th1 response is more sensitive to the level of miR-17-92 expression.Entities:
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Year: 2015 PMID: 26276869 PMCID: PMC5053620 DOI: 10.4049/jimmunol.1500317
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422