Ager A, Fajumi J, Sparshott S M, Ford W L, Butcher G W
Department of Cell and Structural Biology, University of Manchester, United Kingdom.
Transplantation. 1988 Nov;46(5):762-7. doi: 10.1097/00007890-198811000-00025.
Allogeneic lymphocyte cytotoxicity (ALC) describes the elimination of allogeneic lymphocytes in vivo by an NK-related activity. There is evidence that ALC is demonstrable between donor and recipient when these are incompatible at MHC gene loci alone. Since ALC is a property of T cell-deficient nude rats, the role of the MHC in this rejection process needs further study. We have determined the contribution of the MHC to ALC using congenic and recombinant rats. In our analysis we have assumed that ALC involves the recognition of classic alloantigens by clonally distributed effector cells as for other examples of transplant rejection, although this is not yet proved. Strong ALC was measured between congenic rats that differed for MHC genes only. Non-MHC incompatibility alone did not elicit ALC. In the presence of MHC incompatibility the strength of ALC generated in a recipient was dependent on non-MHC genes. The PVG background generated high ALC responses whereas ALC was not measured in the DA rat. However ALC was measured in the congenic PVG-RT1avl (DA) rat. The contributions of classic class I (RT1.A), class II (RT1.B/D), and medial transplantation (RT1.C) regions of the rat MHC were determined by comparing different recombinant donors into the same recipient strain. Single region differences alone in any of these three MHC regions did not elicit full ALC. In two sets of transfers a combination of RT1.B/D and RT1.C region incompatibility was sufficient to generate a full allogeneic response. It can be concluded that the controlling element for allogeneic lymphocyte cytotoxicity is in the RT1.B/D-RT1.C region of the rat MHC.
同种异体淋巴细胞毒性（ALC）描述了自然杀伤相关活性在体内对同种异体淋巴细胞的清除作用。有证据表明，当供体和受体仅在MHC基因位点不相容时，可检测到ALC。由于ALC是T细胞缺陷裸鼠的一种特性，因此MHC在这种排斥过程中的作用需要进一步研究。我们使用同源近交系和重组大鼠确定了MHC对ALC的贡献。在我们的分析中，我们假设ALC涉及克隆分布的效应细胞对经典同种异体抗原的识别，如同其他移植排斥的例子一样，尽管这尚未得到证实。仅在MHC基因不同的同源近交系大鼠之间检测到强烈的ALC。单独的非MHC不相容性不会引发ALC。在存在MHC不相容性的情况下，受体中产生的ALC强度取决于非MHC基因。PVG背景产生高ALC反应，而在DA大鼠中未检测到ALC。然而，在同源近交系PVG-RT1avl（DA）大鼠中检测到了ALC。通过将不同的重组供体与同一受体品系进行比较，确定了大鼠MHC经典的I类（RT1.A）、II类（RT1.B/D）和中间移植（RT1.C）区域的贡献。这三个MHC区域中任何一个单独的单区域差异都不会引发完全的ALC。在两组移植中，RT1.B/D和RT1.C区域不相容性的组合足以产生完全的同种异体反应。可以得出结论：同种异体淋巴细胞毒性的控制元件位于大鼠MHC的RT1.B/D-RT1.C区域。
