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对镍过敏的接触性皮炎患者的T淋巴细胞的直接和间接镍特异性刺激。

Direct and indirect nickel-specific stimulation of T lymphocytes from patients with allergic contact dermatitis to nickel.

作者信息

Kapsenberg M L, Van der Pouw-Kraan T, Stiekema F E, Schootemeijer A, Bos J D

机构信息

Department of Histology and Cell Biology, University of Amsterdam, The Netherlands.

出版信息

Eur J Immunol. 1988 Jul;18(7):977-82. doi: 10.1002/eji.1830180702.

Abstract

Fourteen T lymphocyte clones (TLC) specific for the contact allergen nickel were prepared either from lesional tissue biopsies or from peripheral blood of patients with allergic nickel-contact dermatitis. Two nickel-specific TLC, obtained from lesional tissue, responded to nickel without the participation of antigen-presenting cells (APC). This direct stimulation by nickel was not restricted by major histocompatibility complex-encoded molecules, since antibodies against HLA class I and II molecules did not block nickel-specific proliferation. Proliferation of other nickel-specific TLC was dependent on the presence of APC and was diversely restricted by HLA class II molecules. With one exception, the restriction determinants were present on HLA-DR and HLA-DQ molecules. Four TLC recognized nickel in association with subtypes of these serologically defined molecules. Five TLC seemed to recognize nickel in the context of highly unusual restriction determinants, since their restrictions could not be explained by the function of single polymorphic HLA class II epitopes. The absence of HLA class II restrictions and the occurrence of deviant HLA class II restrictions in part of the nickel-specific TLC are suggested to result from direct interactions of nickel with critical immune response molecules.

摘要

从过敏性镍接触性皮炎患者的皮损组织活检或外周血中制备了14个针对接触性变应原镍的T淋巴细胞克隆(TLC)。从皮损组织中获得的两个镍特异性TLC在无抗原呈递细胞(APC)参与的情况下对镍有反应。镍的这种直接刺激不受主要组织相容性复合体编码分子的限制,因为针对HLA I类和II类分子的抗体不会阻断镍特异性增殖。其他镍特异性TLC的增殖依赖于APC的存在,并受到HLA II类分子的不同限制。除了一个例外,限制决定簇存在于HLA-DR和HLA-DQ分子上。四个TLC识别与这些血清学定义分子的亚型相关的镍。五个TLC似乎在高度不寻常的限制决定簇的背景下识别镍,因为它们的限制不能用单个多态性HLA II类表位的功能来解释。部分镍特异性TLC中HLA II类限制的缺失和异常HLA II类限制的出现被认为是镍与关键免疫反应分子直接相互作用的结果。

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