| First Author | Yang R | Year | 2015 |
| Journal | Elife | Volume | 4 |
| PubMed ID | 25974216 | Mgi Jnum | J:223311 |
| Mgi Id | MGI:5648660 | Doi | 10.7554/eLife.06376 |
| Citation | Yang R, et al. (2015) Mitochondrial Ca(2)(+) and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function. Elife 4 |
| abstractText | IL-6 plays an important role in determining the fate of effector CD4 cells and the cytokines that these cells produce. Here we identify a novel molecular mechanism by which IL-6 regulates CD4 cell effector function. We show that IL-6-dependent signal facilitates the formation of mitochondrial respiratory chain supercomplexes to sustain high mitochondrial membrane potential late during activation of CD4 cells. Mitochondrial hyperpolarization caused by IL-6 is uncoupled from the production of ATP by oxidative phosphorylation. However, it is a mechanism to raise the levels of mitochondrial Ca(2+) late during activation of CD4 cells. Increased levels of mitochondrial Ca(2+) in the presence of IL-6 are used to prolong Il4 and Il21 expression in effector CD4 cells. Thus, the effect of IL-6 on mitochondrial membrane potential and mitochondrial Ca(2+) is an alternative pathway by which IL-6 regulates effector function of CD4 cells and it could contribute to the pathogenesis of inflammatory diseases. |
