| Autor: |
Zhang, Jinyu, Vandevenne, Patricia, Hamdi, Haifa, Puyvelde, Merry, Zucchi, Alessandro, Bettonville, Marie, Weatherly, Kathleen, Braun, Michel Y. |
| Zdroj: |
European Journal of Immunology; Mar2015, Vol. 45 Issue 3, p829-842, 14p |
| Abstrakt: |
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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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