The microRNA miR-31 inhibits CD8 + T cell function in chronic viral infection

Howell F. Moffett, Adam N.R. Cartwright, Hye Jung Kim, Jernej Godec, Jason Pyrdol, Tarmo Äijö, Gustavo J. Martinez, Anjana Rao, Jun Lu, Todd R. Golub, Harvey Cantor, Arlene H. Sharpe, Carl D. Novina, Kai W. Wucherpfennig*

*Corresponding author for this work

Research output: Contribution to journalArticleScientificpeer-review

33 Citations (Scopus)


During infection, antigen-specific T cells undergo tightly regulated developmental transitions controlled by transcriptional and post-transcriptional regulation of gene expression. We found that the microRNA miR-31 was strongly induced by activation of the T cell antigen receptor (TCR) in a pathway involving calcium and activation of the transcription factor NFAT. During chronic infection with lymphocytic choriomeningitis virus (LCMV) clone 13, miR-31-deficent mice recovered from clinical disease, while wild-type mice continued to show signs of disease. This disease phenotype was explained by the presence of larger numbers of cytokine-secreting LCMV-specific CD8 + T cells in miR-31-deficent mice than in wild-type mice. Mechanistically, miR-31 increased the sensitivity of T cells to type I interferons, which interfered with effector T cell function and increased the expression of several proteins related to T cell dysfunction during chronic infection. These studies identify miR-31 as an important regulator of T cell exhaustion in chronic infection.

Original languageEnglish
Pages (from-to)791-799
Number of pages9
Issue number7
Publication statusPublished - 20 Jun 2017
MoE publication typeA1 Journal article-refereed

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