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000137584 1001_ $$aWabnitz, Guido H$$b0
000137584 245__ $$aPP1α and Cofilin regulate nuclear translocation of NFkB and promote expression of the anti-inflammatory cytokine IL-10 by T-cells.
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000137584 520__ $$aWhile several protein serine-threonine kinases control cytokine production by T-cells, the roles of serine-threonine phosphatases are largely unexplored. Here, we analysed the involvement of protein phosphatase-1α (PP1α) in cytokine synthesis following costimulation of primary human T-cells. SiRNA-mediated knock-down of PP1α (PP1KD) or expression of a dominant-negative PP1α (D95N-PP1) drastically diminished IL-10 production. Focusing on a key transcriptional activator of human IL-10, we demonstrate that nuclear translocation of NF-kB was significantly inhibited in PP1KD or D95N-PP1 cells. Interestingly, knockdown of cofilin, a known substrate of PP1 containing a nuclear localization signal, also prevented nuclear accumulation of NF-kB. Expression of a constitutively active non-phosphorylatable S3A-cofilin in D95N-PP1 cells restored nuclear translocation of NF-kB and IL-10 expression. Sub-population analysis revealed that defective nuclear translocation of NF-kB was most prominent in CD4+CD45RA-CXCR3- T-cells that included IL-10-producing TH2 cells. Together these findings reveal novel functions for PP1α and its substrate cofilin in T-cells namely the regulation of the nuclear translocation of NF-kB and promotion of IL-10 production. These data suggest that stimulation of PP1α could limit the overwhelming immune responses seen in chronic inflammatory diseases.
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000137584 7001_ $$aKirchgessner, Henning$$b1
000137584 7001_ $$aJahraus, Beate$$b2
000137584 7001_ $$0P:(DE-He78)d5882ffec9d5dea0104c7d33165e4a45$$aUmansky, Ludmila$$b3$$udkfz
000137584 7001_ $$aShenolikar, Shirish$$b4
000137584 7001_ $$aSamstag, Yvonne$$b5
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000137584 9141_ $$y2018
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