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CD28 Regulates Metabolic Fitness for Long-Lived Plasma Cell Survival.

Abstract：

:Durable humoral immunity against epidemic infectious disease requires the survival of long-lived plasma cells (LLPCs). LLPC longevity is dependent on metabolic programs distinct from short-lived plasma cells (SLPCs); however, the mechanistic basis for this difference is unclear. We have previously shown that CD28, the prototypic T cell costimulatory receptor, is expressed on both LLPCs and SLPCs but is essential only for LLPC survival. Here we show that CD28 transduces pro-survival signaling specifically in LLPCs through differential SLP76 expression. CD28 signaling in LLPCs increased glucose uptake, mitochondrial mass/respiration, and reactive oxygen species (ROS) production. Unexpectedly, CD28-mediated regulation of mitochondrial respiration, NF-κB activation, and survival was ROS dependent. IRF4, a target of NF-κB, was upregulated by CD28 activation in LLPCs and decreased IRF4 levels correlated with decreased glucose uptake, mitochondrial mass, ROS, and CD28-mediated survival. Altogether, these data demonstrate that CD28 signaling induces a ROS-dependent metabolic program required for LLPC survival.

journal_name

Cell Rep

journal_title

Cell reports

authors

Utley A,Chavel C,Lightman S,Holling GA,Cooper J,Peng P,Liu W,Barwick BG,Gavile CM,Maguire O,Murray-Dupuis M,Rozanski C,Jordan MS,Kambayashi T,Olejniczak SH,Boise LH,Lee KP

doi

10.1016/j.celrep.2020.107815

subject

Has Abstract

pub_date

2020-06-23 00:00:00

pages

107815

issue

12

issn

2211-1247

pii

S2211-1247(20)30796-8

journal_volume

31

pub_type

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