Proteomics

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P2X7 signaling drives Th1 cell differentiation through metabolic reprogramming for aerobic glycolysis


ABSTRACT: This study provides evidence on the molecular mechanisms by which P2RX7 signaling promotes Th1 cell differentiation. P2RX7 induces T-bet expression and aerobic glycolysis in splenic CD4+ T cells that respond to malaria, at a time prior to Th1/Tfh polarization. Cell-intrinsic P2RX7 signaling sustains the glycolytic pathway and causes bioenergetic mitochondrial stress in activated CD4+ T cells. We also show in vitro the phenotypic similarities of Th1-polarized CD4+ T cells that do not express P2RX7 and those in which the glycolytic pathway is pharmacologically inhibited. In addition, ATP synthase blockade in vitro and the consequent inhibition of oxidative phosphorylation, which forces cells to use aerobic glycolysis, is sufficient to promote rapid CD4+ T cell proliferation and polarization to the Th1 profile in the absence of P2RX7. These data demonstrate that P2RX7-mediated metabolic reprograming for aerobic glycolysis is a key event for Th1 cell differentiation and suggest that ATP synthase inhibition is a fundamental mechanism by which P2X7 signaling induces the Th1 response.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Spleen

SUBMITTER: Veronica Santiago  

LAB HEAD: Maria Regina D’Império Lima

PROVIDER: PXD037754 | Pride | 2023-03-08

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
erika11_1.raw Raw
erika11_2.raw Raw
erika12_1.raw Raw
erika12_2.raw Raw
erika3_1.raw Raw
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