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Protein phosphatase 2A B55[beta] limits [CD8.sup.+] T cell lifespan following cytokine withdrawal
Ist Teil von
The Journal of clinical investigation, 2020-11, Vol.130 (11), p.5989
Ort / Verlag
American Society for Clinical Investigation
Erscheinungsjahr
2020
Quelle
Free E-Journal (出版社公開部分のみ)
Beschreibungen/Notizen
How T cells integrate environmental cues into signals that limit the magnitude and length of immune responses is poorly understood. Here, we provide data that demonstrate that B55[beta], a regulatory subunit of protein phosphatase 2A, represents a molecular link between cytokine concentration and apoptosis in activated [CD8.sup.+] T cells. Through the modulation of AKT, B55[beta] induced the expression of the proapoptotic molecule Hrk in response to cytokine withdrawal. Accordingly, B55[beta] and Hrk were both required for in vivo and in vitro contraction of activated [CD8.sup.+] lymphocytes. We show that this process plays a role during clonal contraction, establishment of immune memory, and preservation of peripheral tolerance. This regulatory pathway may represent an unexplored opportunity to end unwanted immune responses or to promote immune memory.