| First Author | Zhang J | Year | 2015 |
| Journal | Eur J Immunol | Volume | 45 |
| Issue | 3 | Pages | 829-42 |
| PubMed ID | 25641586 | Mgi Jnum | J:223837 |
| Mgi Id | MGI:5660461 | Doi | 10.1002/eji.201445066 |
| Citation | Zhang J, et al. (2015) Micro-RNA-155-mediated control of heme oxygenase 1 (HO-1) is required for restoring adaptively tolerant CD4+ T-cell function in rodents. Eur J Immunol 45(3):829-42 |
| abstractText | T cells chronically stimulated by a persistent antigen often become dysfunctional and lose effector functions and proliferative capacity. To identify the importance of micro-RNA-155 (miR-155) in this phenomenon, we analyzed mouse miR-155-deficient CD4(+) T cells in a model where the chronic exposure to a systemic antigen led to T-cell functional unresponsiveness. We found that miR-155 was required for restoring function of T cells after programmed death receptor 1 blockade. Heme oxygenase 1 (HO-1) was identified as a specific target of miR-155 and inhibition of HO-1 activity restored the expansion and tissue migration capacity of miR-155(-/-) CD4(+) T cells. Moreover, miR-155-mediated control of HO-1 expression in CD4(+) T cells was shown to sustain in vivo antigen-specific expansion and IL-2 production. Thus, our data identify HO-1 regulation as a mechanism by which miR-155 promotes T-cell-driven inflammation. |
