解析维甲酸受体异构体在感染后 CD8 应答中的作用。
Dissecting the role of retinoic acid receptor isoforms in the CD8 response to infection.
机构信息
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Norris Cotton Cancer Center, Lebanon, NH 03756.
出版信息
J Immunol. 2014 Apr 1;192(7):3336-44. doi: 10.4049/jimmunol.1301949. Epub 2014 Mar 7.
Abstract
Vitamin A deficiency leads to increased susceptibility to a spectrum of infectious diseases. The studies presented dissect the intrinsic role of each of the retinoic acid receptor (RAR) isoforms in the clonal expansion, differentiation, and survival of pathogen-specific CD8 T cells in vivo. The data show that RARα is required for the expression of gut-homing receptors on CD8(+) T cells and survival of CD8(+) T cells in vitro. Furthermore, RARα is essential for survival of CD8(+) T cells in vivo following Listeria monocytogenes infection. In contrast, RARβ deletion leads to modest deficiency in Ag-specific CD8(+) T cell expansion during infection. The defective survival of RARα-deficient CD8(+) T cells leads to a deficiency in control of L. monocytogenes expansion in the spleen. To our knowledge, these are the first comparative studies of the role of RAR isoforms in CD8(+) T cell immunity.
摘要
维生素 A 缺乏会导致对一系列传染病的易感性增加。本研究阐述了视黄酸受体（RAR）异构体在体内病原体特异性 CD8 T 细胞克隆扩增、分化和存活中的固有作用。数据表明，RARα对于 CD8(+)T 细胞上归巢受体的表达和 CD8(+)T 细胞的体外存活是必需的。此外，RARα对于李斯特菌感染后 CD8(+)T 细胞的体内存活也是必需的。相比之下，RARβ 缺失导致感染期间 Ag 特异性 CD8(+)T 细胞扩增的适度缺陷。RARα 缺陷的 CD8(+)T 细胞的存活缺陷导致对李斯特菌在脾脏中扩张的控制不足。据我们所知，这些是 RAR 异构体在 CD8(+)T 细胞免疫中作用的首次比较研究。
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