Phosphatidylinositol-3-OH kinase and nutrient-sensing mTOR pathways control T lymphocyte trafficking.
Phosphatidylinositol-3-OH kinase and nutrient-sensing mTOR pathways control T lymphocyte trafficking.
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PI 3 K和mTOR是进化上保守的细胞代谢调节剂。在这里，我们显示PI 3 K和mTOR决定T淋巴细胞表达的粘附和趋化因子受体的库。关键淋巴结归巢受体CD 62 L（L-选择素）和CCR 7在初始T淋巴细胞上高度表达，但在免疫激活后下调。CD 62 L下调通过胞外域蛋白水解和基因转录抑制发生。PI 3 K p110δ通过丝裂原活化蛋白（MAP）激酶控制CD 62 L蛋白水解，而PI 3 K p110δ对CD 62 L转录的控制由营养传感器mTOR通过转录因子KLF 2的调节介导。PI 3 K-mTOR营养传感途径还决定了趋化因子受体CCR 7的表达并调节体内淋巴细胞运输。因此，淋巴细胞利用PI 3 K和mTOR来匹配代谢和运输。
PI3K and mTOR are evolutionarily conserved regulators of cell metabolism. Here we show PI3K and mTOR determine the repertoire of adhesion and chemokine receptors expressed by T lymphocytes. Key lymph node homing receptors, CD62L (L-selectin) and CCR7, are highly expressed on naive T lymphocytes but downregulated following immune activation. CD62L downregulation occurs via ectodomain proteolysis and suppression of gene transcription. PI3K p110δ controls CD62L proteolysis via mitogen-activated protein (MAP) kinases whereas PI3K p110δ control of CD62L transcription is mediated by the nutrient sensor mTOR via regulation of the transcription factor KLF2. PI3K-mTOR nutrient sensing pathways also determined expression of the chemokine receptor CCR7 and regulate lymphocyte trafficking in vivo. Hence, lymphocytes utilize PI3K and mTOR to match metabolism and trafficking.
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