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与T细胞MHC限制位点相关的表位。I. I-A表位在H-2限制的辅助性T细胞上的选择性表达。

Epitopes associated with the MHC restriction site of T cells. I. Selective expression of Iat epitopes on H-2-restricted helper T cells.

作者信息

Abe R, Yagi J, Asano Y, Tada T

出版信息

J Immunol. 1987 May 1;138(9):2964-9.

PMID:2437200
Abstract

We previously established monoclonal antibodies (mAb) that are putatively directed to the I region of H-2k but are reactive only with T cells. Because of their specificity to the unique epitopes different from class II antigens, they are designated as anti-Iat reagents. The present study demonstrated that these anti-Iat inhibit the H-2k-restricted helper T (Th) cell function by acting on the very H-2 restriction site of both H-2k and H-2kxb F1 T cells. This was determined by both the cytotoxic treatment and blocking of antigen-primed Th cells. In the F1 Th population, only those restricted to H-2k were eliminated, leaving the H-2b-restricted Th cells uninhibited. The inhibition of the response was not due to the induction of suppressor T cells, but to the elimination of the function of radioresistant Lyt-1+,2- Th cells. Iatk epitopes were also found on an H-2k-restricted but not on H-2b-restricted Th cell clone established from the same H-2kxb F1 animal. None of the anti-Iatk were reactive with class II antigens on B cells. These results indicate that Iat epitopes are not directly encoded by the I region genes, but are associated with the H-2 restriction site of T cells, which see the self class II polymorphism. Thus, Iat epitopes are expressed clonally in high frequency on H-2k-restricted Th cells of F1, being excluded from the H-2b-restricted Th population. The relationship between Iat and T cell receptor molecules is unknown.

摘要

我们之前制备了单克隆抗体(mAb),这些抗体被认为是针对H-2k的I区,但仅与T细胞发生反应。由于它们对不同于II类抗原的独特表位具有特异性,因此被指定为抗-Iat试剂。本研究表明,这些抗-Iat通过作用于H-2k和H-2kxb F1 T细胞的H-2限制位点来抑制H-2k限制的辅助性T(Th)细胞功能。这是通过对抗原致敏的Th细胞进行细胞毒性处理和阻断来确定的。在F1 Th群体中,只有那些受H-2k限制的细胞被清除,而受H-2b限制的Th细胞未受抑制。反应的抑制不是由于抑制性T细胞的诱导,而是由于消除了辐射抗性Lyt-1 +,2- Th细胞的功能。Iatk表位也在从同一H-2kxb F1动物建立的H-2k限制而非H-2b限制的Th细胞克隆上被发现。没有一种抗-Iatk与B细胞上的II类抗原发生反应。这些结果表明,Iat表位不是由I区基因直接编码的,而是与T细胞的H-2限制位点相关,该位点能识别自身II类多态性。因此,Iat表位在F1的H-2k限制的Th细胞上以高频率克隆表达,而被排除在H-2b限制的Th群体之外。Iat与T细胞受体分子之间的关系尚不清楚。

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