| First Author | Moffett HF | Year | 2017 |
| Journal | Nat Immunol | Volume | 18 |
| Issue | 7 | Pages | 791-799 |
| PubMed ID | 28530712 | Mgi Jnum | J:259150 |
| Mgi Id | MGI:6142308 | Doi | 10.1038/ni.3755 |
| Citation | Moffett HF, et al. (2017) The microRNA miR-31 inhibits CD8(+) T cell function in chronic viral infection. Nat Immunol 18(7):791-799 |
| abstractText | 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. |
