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CD69通过LAT1-CD98控制L-色氨酸的摄取以及在银屑病中通过芳烃受体依赖途径分泌白细胞介素-22。

CD69 controls the uptake of L-tryptophan through LAT1-CD98 and AhR-dependent secretion of IL-22 in psoriasis.

作者信息

Cibrian Danay, Saiz María Laura, de la Fuente Hortensia, Sánchez-Díaz Raquel, Moreno-Gonzalo Olga, Jorge Inmaculada, Ferrarini Alessia, Vázquez Jesús, Punzón Carmen, Fresno Manuel, Vicente-Manzanares Miguel, Daudén Esteban, Fernández-Salguero Pedro M, Martín Pilar, Sánchez-Madrid Francisco

机构信息

Immunology Service, Hospital de la Princesa, Universidad Autónoma de Madrid, Instituto Investigación Sanitaria Princesa, Madrid, Spain.

Department of Vascular Biology and Inflammation, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.

出版信息

Nat Immunol. 2016 Aug;17(8):985-96. doi: 10.1038/ni.3504. Epub 2016 Jul 4.

DOI:10.1038/ni.3504
PMID:27376471
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5146640/
Abstract

The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydrocarbon receptor (AhR)-dependent secretion of interleukin 22 (IL-22) by γδ T cells, which contributed to the development of psoriasis induced by IL-23. CD69 associated with the aromatic-amino-acid-transporter complex LAT1-CD98 and regulated its surface expression and uptake of L-tryptophan (L-Trp) and the intracellular quantity of L-Trp-derived activators of AhR. In vivo administration of L-Trp, an inhibitor of AhR or IL-22 abrogated the differences between CD69-deficient mice and wild-type mice in skin inflammation. We also observed LAT1-mediated regulation of AhR activation and IL-22 secretion in circulating Vγ9(+) γδ T cells of psoriatic patients. Thus, CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98-mediated metabolic cues.

摘要

活化标志物CD69由皮肤γδT细胞表达。我们在此发现，CD69控制γδT细胞中芳烃受体（AhR）依赖性白细胞介素22（IL-22）的分泌，这有助于IL-23诱导的银屑病的发展。CD69与芳香族氨基酸转运体复合物LAT1-CD98相关联，并调节其表面表达以及L-色氨酸（L-Trp）的摄取和AhR的L-Trp衍生激活剂的细胞内含量。在体内给予L-Trp、AhR抑制剂或IL-22可消除CD69缺陷小鼠和野生型小鼠在皮肤炎症方面的差异。我们还观察到银屑病患者循环Vγ9(+)γδT细胞中LAT1介导的AhR激活和IL-22分泌的调节。因此，CD69通过控制LAT1-CD98介导的代谢线索，作为银屑病发病机制的关键介质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7468/5146640/399190b46595/emss-69726-f008.jpg
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