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紫外线B辐射诱导的抑制性T淋巴细胞的起源与特性

Origin and characteristics of ultraviolet-B radiation-induced suppressor T lymphocytes.

作者信息

Shreedhar V K, Pride M W, Sun Y, Kripke M L, Strickland F M

机构信息

Department of Immunology, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.

出版信息

J Immunol. 1998 Aug 1;161(3):1327-35.

PMID:9686595
Abstract

Cutaneous exposure to low dose (2 kJ/m2) ultraviolet B radiation impairs the induction of contact hypersensitivity (CHS) responses to haptens applied to UV-irradiated skin and induces hapten-specific suppressor T lymphocytes (Ts). Cells collected from the draining lymph nodes of UV-irradiated, FITC-sensitized mice have impaired Ag-presenting activity and induce Ts cells upon injection into syngeneic recipients. This study investigates whether Ts cells originate in the UV-irradiated donor mice or are induced in lymph node cell recipients and the mechanism of suppression. Using congenic mice, we determined that the Ts cells in recipient animals were derived from T cells in the draining lymph nodes of the UV-irradiated donors. Cell lines and clones established from unirradiated and UV-irradiated, FITC-sensitized mice were CD4+, CD8-, TCR-alpha/beta+, MHC restricted, and hapten specific. The T cells proliferated in response to APC sensitized in vivo, but not to APC coupled in vitro with FITC. Cell lines from unirradiated mice were Th1 like, producing large amounts of IFN-gamma, but little IL-4 or IL-10, whereas cloned Ts cells from UV-irradiated mice produced IL-10, but no IL-4 or IFN-gamma. Ts cells blocked APC functions and IL-12 production in vitro. Injection of 5 x 10(4) cloned Ts cells into untreated recipients suppressed the induction of CHS. These results suggest that UV radiation can induce a distinct T regulatory type 1-like Ts population that may block the activation of Th1 cell-mediated immune responses.

摘要

皮肤暴露于低剂量(2 kJ/m²)的紫外线B辐射会损害对施加于紫外线照射皮肤的半抗原的接触性超敏反应(CHS)的诱导,并诱导半抗原特异性抑制性T淋巴细胞(Ts)。从紫外线照射、异硫氰酸荧光素(FITC)致敏小鼠的引流淋巴结中收集的细胞具有受损的抗原呈递活性,并在注射到同基因受体中时诱导Ts细胞。本研究调查Ts细胞是起源于紫外线照射的供体小鼠还是在淋巴结细胞受体中诱导产生,以及抑制机制。使用同源基因小鼠,我们确定受体动物中的Ts细胞源自紫外线照射供体的引流淋巴结中的T细胞。从未照射和紫外线照射、FITC致敏小鼠建立的细胞系和克隆是CD4+、CD8-、TCR-α/β+、MHC受限且半抗原特异性的。T细胞对体内致敏的抗原呈递细胞(APC)有增殖反应,但对体外与FITC偶联的APC无增殖反应。未照射小鼠的细胞系类似Th1,产生大量干扰素-γ,但很少白细胞介素-4或白细胞介素-10,而来自紫外线照射小鼠的克隆Ts细胞产生白细胞介素-10,但不产生白细胞介素-4或干扰素-γ。Ts细胞在体外阻断APC功能和白细胞介素-12的产生。将5×10⁴个克隆的Ts细胞注射到未处理的受体中可抑制CHS的诱导。这些结果表明,紫外线辐射可诱导一种独特的1型调节性T样Ts细胞群体,该群体可能阻断Th1细胞介导的免疫反应的激活。

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