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细胞毒性人血淋巴细胞上表达的细胞间黏附分子-1(CD54)的功能特性

Functional characteristics of the intercellular adhesion molecule-1 (CD54) expressed on cytotoxic human blood lymphocytes.

作者信息

Wang P, Vánky F, Li S L, Patarroyo M, Klein E

机构信息

Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.

出版信息

Cell Immunol. 1990 Dec;131(2):366-80. doi: 10.1016/0008-8749(90)90261-o.

Abstract

We have shown that intercellular adhesion molecule-1 (ICAM-1) (CD54) positive cells are mainly responsible for the natural cytotoxic function of human blood lymphocytes. The evidences were the inhibition of cytotoxicity by anti-ICAM-1 (LB-2) monoclonal antibodies (mAb) and the loss of lytic activity after removal of the ICAM-1+ cells. In addition, the cytotoxic potential of the separated ICAM-1- lymphocyte population after activation appeared in parallel with the expression of this molecule. The ICAM-1+ lymphocytes lysed both LFA-1 (CD11a/CD18 or Leu-CAMa) positive and negative cell lines, and pretreatment of the effectors with the LB-2 mAb also inhibited the lysis of LFA-1- targets. The results point to a yet unrecognized role of ICAM-1 on the lymphocytes. Kinetics experiments suggested that pretreatment of lymphocytes with alpha-ICAM-1 (LB-2) mAb did not inhibit the promptly established lytic interactions but influenced later events, recycling and/or recruitment of effectors. It is possible that the cytotoxic potential is regulated by contacts between the members of the lymphocyte population and that these events occur via their ICAM-1 and LFA-1. Exposure of lymphocytes to NK-sensitive targets for 16 hr elevated their cytotoxic potential. The function of activated lymphocytes was not inhibited by the LB-2 mAb.

摘要

我们已经表明,细胞间黏附分子-1(ICAM-1)(CD54)阳性细胞主要负责人类血液淋巴细胞的天然细胞毒性功能。证据包括抗ICAM-1(LB-2)单克隆抗体(mAb)对细胞毒性的抑制作用以及去除ICAM-1+细胞后裂解活性的丧失。此外,分离的ICAM-1-淋巴细胞群体激活后的细胞毒性潜力与该分子的表达平行出现。ICAM-1+淋巴细胞可裂解LFA-1(CD11a/CD18或Leu-CAMa)阳性和阴性细胞系,用LB-2 mAb预处理效应细胞也可抑制对LFA-1阴性靶细胞的裂解。结果表明ICAM-1在淋巴细胞上具有尚未被认识的作用。动力学实验表明,用α-ICAM-1(LB-2)mAb预处理淋巴细胞不会抑制迅速建立的裂解相互作用,但会影响后续事件,即效应细胞的再循环和/或募集。细胞毒性潜力可能受淋巴细胞群体成员之间的接触调节,并且这些事件通过它们的ICAM-1和LFA-1发生。将淋巴细胞与NK敏感靶细胞接触16小时可提高其细胞毒性潜力。活化淋巴细胞的功能不受LB-2 mAb的抑制。

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