| First Author | Ma F | Year | 2011 |
| Journal | Nat Immunol | Volume | 12 |
| Issue | 9 | Pages | 861-9 |
| PubMed ID | 21785411 | Mgi Jnum | J:176470 |
| Mgi Id | MGI:5291887 | Doi | 10.1038/ni.2073 |
| Citation | Ma F, et al. (2011) The microRNA miR-29 controls innate and adaptive immune responses to intracellular bacterial infection by targeting interferon-gamma. Nat Immunol 12(9):861-9 |
| abstractText | Interferon-gamma (IFN-gamma) has a critical role in immune responses to intracellular bacterial infection. MicroRNAs (miRNAs) are important in the regulation of innate and adaptive immunity. However, whether miRNAs can directly target IFN-gamma and regulate IFN-gamma production post-transcriptionally remains unknown. Here we show that infection of mice with Listeria monocytogenes or Mycobacterium bovis bacillus Calmette-Guerin (BCG) downregulated miR-29 expression in IFN-gamma-producing natural killer cells, CD4(+) T cells and CD8(+) T cells. Moreover, miR-29 suppressed IFN-gamma production by directly targeting IFN-gamma mRNA. We developed mice with transgenic expression of a 'sponge' target to compete with endogenous miR-29 targets (GS29 mice). We found higher serum concentrations of IFN-gamma and lower L. monocytogenes burdens in L. monocytogenes-infected GS29 mice than in their littermates. GS29 mice had enhanced T helper type 1 (T(H)1) responses and greater resistance to infection with BCG or Mycobacterium tuberculosis. Therefore, miR-29 suppresses immune responses to intracellular pathogens by targeting IFN-gamma. |
