有哪些信誉好的足球投注网站activated human cd4+cd45ro+ memory t-cells indirectly inhibit nlrp3 inflammasome activation through downregulation of p2x7r signalling激活人类的cd4 + cd45ro +记忆t细胞间接抑制nlrp3 inflammasome激活p2x7r的差别通过对这些信号.pdfVIP
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activatedhumancd4cd45romemoryt-cellsindirectlyinhibitnlrp3inflammasomeactivationthroughdownregulationofp2x7rsignalling激活人类的cd4cd45ro记忆t细胞间接抑制nlrp3inflammasome激活p2x7r的差别通过对这些信号
Activated Human CD4+CD45RO+ Memory T-Cells
Indirectly Inhibit NLRP3 Inflammasome Activation
through Downregulation of P2X7R Signalling
Vanessa Beynon, Francisco J. Quintana, Howard L. Weiner*
Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
Abstract
Inflammasomes are multi-protein complexes that control the production of pro-inflammatory cytokines such as IL-1b.
Inflammasomes play an important role in the control of immunity to tumors and infections, and also in autoimmune
diseases, but the mechanisms controlling the activation of human inflammasomes are largely unknown. We found that
human activated CD4+CD45RO+ memory T-cells specifically suppress P2X7R-mediated NLRP3 inflammasome activation,
without affecting P2X7R-independent NLRP3 or NLRP1 inflammasome activation. The concomitant increase in pro-IL-1b
production induced by activated memory T-cells concealed this effect. Priming with IFNb decreased pro-IL-1b production in
addition to NLRP3 inflammasome inhibition and thus unmasked the inhibitory effect on NLRP3 inflammasome activation.
IFNb suppresses NLRP3 inflammasome activation through an indirect mechanism involving decreased P2X7R signaling. The
inhibition of pro-IL-1b production and suppression of NLRP3 inflammasome activation by IFNb-primed human
CD4+CD45RO+ memory T-cells is partly mediated by soluble FasL and is associated with down-regulated P2X7R mRNA
expression and reduced response to ATP in monocytes. CD4+CD45RO+ memory T-cells from multiple sclerosis (MS) patients
showed a reduced ability to suppress NLRP3 inflammasome activation, however their suppressive ability was recovered
following in vivo treatment with IFNb. Thus, our data dem
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