Suppr超能文献

使用针对人T辅助细胞的单克隆抗体分离自体和异体混合淋巴细胞反应性。

Dissociation of autologous and allogeneic mixed lymphocyte reactivity by using a monoclonal antibody specific for human T helper cells.

作者信息

Ellis T M, Mohanakumar T

出版信息

J Immunol. 1983 Nov;131(5):2323-7.

PMID:6226740
Abstract

A monoclonal antibody defining a population of human T helper cells was developed and shown to specifically block the autologous mixed lymphocyte reaction (AMLR). This antibody, termed KT69-7 (IgG1), recognized 62% of peripheral blood E rosette-positive (E+) cells while demonstrating negligible reactivity with E- cells, monocytes, granulocytes, EBV-transformed B cell lines, and mouse splenocytes. Separation of E+ cells into KT69-7+ and KT69-7- populations revealed that KT69-7+ T cells provided helper function in PWM-driven B cell differentiation, whereas KT69-7- T cells provided no help and may suppress this response. Modulation of membrane moieties by using KT69-7 or OKT4 plus goat anti-mouse IgG removed reactivity to both these antibodies, suggesting an association between these molecules recognized by these antibodies. In functional studies, KT69-7 selectively blocked the AMLR while demonstrating minimal or no effect on the allogeneic MLR (allo-MLR). Blocking of the autoreactivity occurred when either autologous B lymphocytes or macrophages were used as stimulators. The failure of KT69-7 to block the allo-MLR was not attributable to excessive allogeneic stimulus; KT69-7 failed to block even under conditions of limiting numbers of stimulator cells. KT69-7 thus appears to recognize a molecule on the surface of T helper cells required for recognition of autologous class II antigens.

摘要

一种鉴定人类辅助性T细胞群体的单克隆抗体被研制出来,并被证明能特异性阻断自体混合淋巴细胞反应(AMLR)。这种抗体被称为KT69-7(IgG1),可识别62%的外周血E花环阳性(E+)细胞,而与E-细胞、单核细胞、粒细胞、EB病毒转化的B细胞系及小鼠脾细胞的反应性可忽略不计。将E+细胞分离为KT69-7+和KT69-7-群体后发现,KT69-7+ T细胞在PWM驱动的B细胞分化中发挥辅助功能,而KT69-7- T细胞则无辅助作用,且可能抑制这种反应。使用KT69-7或OKT4加山羊抗小鼠IgG调节膜成分可消除对这两种抗体的反应性,提示这些抗体识别的分子之间存在关联。在功能研究中,KT69-7选择性阻断AMLR,而对同种异体混合淋巴细胞反应(allo-MLR)的影响极小或无影响。当使用自体B淋巴细胞或巨噬细胞作为刺激细胞时,可阻断自身反应性。KT69-7不能阻断allo-MLR并非由于同种异体刺激过度;即使在刺激细胞数量有限的条件下,KT69-7也无法阻断。因此,KT69-7似乎识别辅助性T细胞表面一种识别自体II类抗原所需的分子。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验