Cutting edge: MIR-17-92 is required for both CD4 Th1 and T follicular helper cell responses during viral infection

Tuoqi Wu, Andreas Wieland, Judong Lee, J. Scott Hale, Jin Hwan Han, Xiaojin Xu, Rafi Ahmed

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

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 virusspecific 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.

Original languageEnglish (US)
Pages (from-to)2515-2519
Number of pages5
JournalJournal of Immunology
Volume195
Issue number6
DOIs
StatePublished - Sep 15 2015
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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