T cell receptor (TCR) signaling without CD28 can elicit primary effector T cells, but memory T cells generated during this process are anergic, failing to respond to secondary antigen exposure. We show that, upon T cell activation, CD28 transiently promotes expression of carnitine palmitoyltransferase 1a (Cpt1a), an enzyme that facilitates mitochondrial fatty acid oxidation (FAO), before the first cell division, coinciding with mitochondrial elongation and enhanced spare respiratory capacity (SRC). microRNA-33 (miR33), a target of thioredoxin-interacting protein (TXNIP), attenuates Cpt1a expression in the absence of CD28, resulting in cells that thereafter are metabolically compromised during reactivation or periods of increased bioenergetic demand. Early CD28-dependent mitochondrial engagement is needed for T cells to remodel cristae, develop SRC, and rapidly produce cytokines upon restimulation-cardinal features of protective memory T cells. Our data show that initial CD28 signals during T cell activation prime mitochondria with latent metabolic capacity that is essential for future T cell responses.

中文翻译：

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CD28引发线粒体。

没有CD28的T细胞受体（TCR）信号传导可以诱导初级效应T细胞，但是在此过程中产生的记忆T细胞是无反应的，不能对次级抗原暴露做出反应。我们显示，在T细胞活化后，CD28瞬时促进肉碱棕榈酰转移酶1a（Cpt1a）的表达，这是一种促进线粒体脂肪酸氧化（FAO）的酶，在第一次细胞分裂之前，与线粒体伸长和增强的备用呼吸能力（SRC）一致）。microRNA-33（miR33）是硫氧还蛋白相互作用蛋白（TXNIP）的靶标，可在CD28不存在的情况下减弱Cpt1a的表达，从而导致其后在激活或生物能需求增加期间代谢受损的细胞。T细胞需要早期CD28依赖的线粒体参与才能重塑cr，发展SRC，并且在保护性记忆T细胞的再刺激基本特征上迅速产生细胞因子。我们的数据表明，在T细胞活化过程中，初始CD28信号会启动具有潜在代谢能力的线粒体，这对于以后的T细胞反应至关重要。