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Mitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function.
Yang, Rui Lirussi, Dario Thornton, Tina M Jelley-Gibbs, Dawn M Diehl, Sean A Case, Laure K Madesh, Muniswamy Taatjes, Douglas J Teuscher, Cory Haynes, Laura
Yang, Rui
Lirussi, Dario
Thornton, Tina M
Jelley-Gibbs, Dawn M
Diehl, Sean A
Case, Laure K
Madesh, Muniswamy
Taatjes, Douglas J
Teuscher, Cory
Haynes, Laura
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Abstract
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.
Citation
Mitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function. 2015, 4: Elife
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PubMed ID
PubMed Central ID
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Article
Language
en
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ISSN
2050-084X