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高剂量UV-B辐射会改变人类树突状细胞的共刺激活性,但在体外并不能使树突状细胞诱导T淋巴细胞对同种异体抗原产生耐受。

High-dose UV-B radiation alters human dendritic cell costimulatory activity but does not allow dendritic cells to tolerize T lymphocytes to alloantigen in vitro.

作者信息

Young J W, Baggers J, Soergel S A

机构信息

Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, NY 10021.

出版信息

Blood. 1993 Jun 1;81(11):2987-97.

PMID:8098966
Abstract

Human blood dendritic cells require UV-B radiation (290 to 320 nm) in excess of 1,000 J/m2 to inhibit their stimulation of primary T-cell responses to alloantigen by 60% to 70% or more. The effect is twofold to threefold greater in the allogeneic mixed leukocyte reaction (MLR) than in polyclonal mitogenesis using comparable numbers of dendritic cells and doses of UV-B radiation. UV-B radiation does not significantly alter dendritic cell viability at the doses administered. Dendritic cell expression of important costimulatory ligands, eg, B7/BB1 and ICAM-1/CD54, is reduced in proportion to the dose of UV-B light administered. UV-B irradiated dendritic cells nevertheless initiate stable contacts with primary alloreactive T lymphocytes that are sufficient to prime T-cell responsiveness to interleukin-2 (IL-2). Subsequent proliferation is severely abrogated without supplemental lymphokine, while T-cell alloreactivity is preserved in a secondary response, irrespective of primary exposure to UV-B irradiated dendritic cells.

摘要

人类血液中的树突状细胞需要超过1000 J/m²的UV-B辐射(290至320纳米),才能将其对同种异体抗原刺激的初级T细胞反应抑制60%至70%或更多。在同种异体混合淋巴细胞反应(MLR)中,使用相当数量的树突状细胞和UV-B辐射剂量时,这种效应比在多克隆有丝分裂中要大两到三倍。在所施用的剂量下,UV-B辐射不会显著改变树突状细胞的活力。重要共刺激配体(如B7/BB1和ICAM-1/CD54)的树突状细胞表达会随着UV-B光施用剂量的增加而按比例降低。然而,经UV-B照射的树突状细胞仍会与初级同种异体反应性T淋巴细胞建立稳定接触,这足以启动T细胞对白介素-2(IL-2)的反应性。在没有补充淋巴因子的情况下,随后的增殖会严重受阻,而T细胞同种异体反应性在二次反应中得以保留,无论初次是否接触经UV-B照射的树突状细胞。

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