Mitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function.

2.50
Hdl Handle:
http://hdl.handle.net/10033/579603
Title:
Mitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function.
Authors:
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; Rincón, Mercedes
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.
Affiliation:
Helmholtz Centre for infection research, Inhoffenstr. 7, D-38124 Braunschweig, Germany.
Citation:
Mitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function. 2015, 4: Elife
Journal:
eLife
Issue Date:
2015
URI:
http://hdl.handle.net/10033/579603
DOI:
10.7554/eLife.06376
PubMed ID:
25974216
Type:
Article
Language:
en
ISSN:
2050-084X
Appears in Collections:
publications of the research group vaccinology and applied microbiology (VAC)

Full metadata record

DC FieldValue Language
dc.contributor.authorYang, Ruien
dc.contributor.authorLirussi, Darioen
dc.contributor.authorThornton, Tina Men
dc.contributor.authorJelley-Gibbs, Dawn Men
dc.contributor.authorDiehl, Sean Aen
dc.contributor.authorCase, Laure Ken
dc.contributor.authorMadesh, Muniswamyen
dc.contributor.authorTaatjes, Douglas Jen
dc.contributor.authorTeuscher, Coryen
dc.contributor.authorHaynes, Lauraen
dc.contributor.authorRincón, Mercedesen
dc.date.accessioned2015-10-13T14:30:44Zen
dc.date.available2015-10-13T14:30:44Zen
dc.date.issued2015en
dc.identifier.citationMitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function. 2015, 4: Elifeen
dc.identifier.issn2050-084Xen
dc.identifier.pmid25974216en
dc.identifier.doi10.7554/eLife.06376en
dc.identifier.urihttp://hdl.handle.net/10033/579603en
dc.description.abstractIL-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.en
dc.language.isoenen
dc.titleMitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for infection research, Inhoffenstr. 7, D-38124 Braunschweig, Germany.en
dc.identifier.journaleLifeen

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