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由编码非经典I类抗原的主要组织相容性复合体区域对大鼠自然杀伤细胞介导的同种异体识别的控制。

Control of rat natural killer cell-mediated allorecognition by a major histocompatibility complex region encoding nonclassical class I antigens.

作者信息

Vaage J T, Naper C, Løvik G, Lambracht D, Rehm A, Hedrich H J, Wonigeit K, Rolstad B

机构信息

Department of Anatomy, University of Oslo, Norway.

出版信息

J Exp Med. 1994 Aug 1;180(2):641-51. doi: 10.1084/jem.180.2.641.

Abstract

The ability of natural killer (NK) cells to eliminate normal allogeneic hemic cells is well established in several species including mice, rats, and humans. The controlling elements for NK susceptibility in these species map to the major histocompatibility complex (MHC), but in contrast to findings in mice and humans, the mode of inheritance is not always recessive in rats. This finding is not easily explained by the missing self and hemopoietic histocompatibility (Hh) models for NK recognition, and has led to the idea that certain alloantigens may trigger NK cell reactivity. In our in vitro system for assessing rat NK alloreactivity, we have employed target and inhibitor cells from a large panel of MHC congenic, intra-MHC recombinant and MHC mutant rat strains, as well as appropriate F1 hybrids between them, and we show the following: (a) The nonclassical class I (RT1.C) region was most important in determining the susceptibility of target cells to alloreactive NK cells in vitro. Lymphocyte susceptibility to lysis in vivo also mapped to the C region, which supports the concept that the in vivo and in vitro alloreactivity assays reflect the same recognition process. (b) Four different RT1-controlled NK allospecificities (represented by the u, l, a, and n haplotypes) could be discerned when we used polyclonal NK cells from the PVG (RT1c) strain as effector cells. Three of the target specificities recognized were controlled mainly by the RT1.C region. (c) The expression of RT1.C region-controlled parental strain NK allodeterminants could be demonstrated in F1 hybrids heterozygous for the C region alone and were therefore inherited nonrecessively. (d) Loss of an RT1.C region-controlled NK allospecificity could be shown with the MHC mutant LEW.1LM1 rat strain characterized by a genomic deletion of about 100 kb of the C region. Taken together, these observations have demonstrated a major importance of the nonclassical class I region, i.e., RT1.C, in controlling rat NK allorecognition, and have thereby assigned a hitherto undescribed immunological property to this region. Furthermore, some of the present data are consistent with the existence of polymorphic NK-triggering alloantigens that are coded for by the RT1.C region.

摘要

自然杀伤(NK)细胞消除正常异基因血细胞的能力在包括小鼠、大鼠和人类在内的多个物种中已得到充分证实。这些物种中NK易感性的控制元件定位于主要组织相容性复合体(MHC),但与小鼠和人类的研究结果不同,大鼠的遗传模式并不总是隐性的。这一发现难以用NK识别的“缺失自我”和造血组织相容性(Hh)模型来解释,由此产生了一种观点,即某些同种异体抗原可能触发NK细胞反应性。在我们评估大鼠NK同种异体反应性的体外系统中,我们使用了来自大量MHC同源、MHC内重组和MHC突变大鼠品系的靶细胞和抑制细胞,以及它们之间合适的F1杂种,我们展示了以下内容:(a)非经典I类(RT1.C)区域在体外确定靶细胞对同种异体反应性NK细胞的易感性方面最为重要。淋巴细胞在体内对裂解的易感性也定位于C区域,这支持了体内和体外同种异体反应性测定反映相同识别过程的概念。(b)当我们使用来自PVG(RT1c)品系的多克隆NK细胞作为效应细胞时,可以辨别出四种不同的由RT1控制的NK同种特异性(由u、l、a和n单倍型代表)。所识别的三种靶特异性主要由RT1.C区域控制。(c)RT1.C区域控制的亲本品系NK同种决定簇的表达可以在仅C区域杂合的F1杂种中得到证实,因此是非隐性遗传的。(d)通过以C区域约100 kb的基因组缺失为特征的MHC突变LEW.1LM1大鼠品系,可以显示RT1.C区域控制的NK同种特异性的丧失。综上所述,这些观察结果证明了非经典I类区域,即RT1.C,在控制大鼠NK同种识别中的重要作用,从而赋予了该区域一种迄今未描述的免疫学特性。此外,目前的一些数据与存在由RT1.C区域编码的多态性NK触发同种异体抗原相一致。

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