Sheehy M J, Mawas C, Charmot D
J Immunol. 1979 Jun;122(6):2198-203.
Human lymphocytes from person A, primed for 10 to 14 days in MLC against lymphocytes from person B, inhibit specifically the proliferative response to B by fresh (i.e., unprimed) lymphocytes of A. Gamma-irradiated (2000 R) primed lymphocytes likewise inhibit specifically, although less strongly. Cells of A, primed with cells of B and then irradiated, usually can inhibit the response of A to cells of any individual sharing HLA-D antigens with B, and the effect tends to be independent of the number of stimulating cells. We also often see inhibition of responses to cells sharing HLA-A and -B antigens with person B, but this effect tends to be lost when the number of stimulating cells is increased. Similarly, at low doses, cells primed for HLA-D antigen a appear not to inhibit the response to an irrelevant HLA-D antigen b on the same stimulating cell. At higher doses of primed cells, even the response to the irrelevant antigen is inhibited. These data suggest to us that at least two mechnaisms may be involved: one directed at the stimulating cell (most likely cell-mediated cytolysis), and predominant at high ratios of primed cells to stimulating cells; the other directed at specific clones of responding cells, and predominant at low ratios.
来自个体A的人淋巴细胞，在混合淋巴细胞培养（MLC）中针对个体B的淋巴细胞致敏10至14天，可特异性抑制A的新鲜（即未致敏）淋巴细胞对B的增殖反应。经γ射线照射（2000伦琴）的致敏淋巴细胞同样具有特异性抑制作用，不过作用较弱。用B的细胞致敏后再经照射的A细胞，通常能够抑制A对任何与B共享HLA - D抗原的个体细胞的反应，且这种效应往往与刺激细胞的数量无关。我们还经常看到对与个体B共享HLA - A和 - B抗原的细胞反应的抑制，但当刺激细胞数量增加时，这种效应往往会消失。同样，在低剂量时，针对HLA - D抗原a致敏的细胞似乎不会抑制对同一刺激细胞上无关的HLA - D抗原b的反应。在高剂量的致敏细胞情况下，甚至对无关抗原的反应也会受到抑制。这些数据向我们表明，可能涉及至少两种机制：一种针对刺激细胞（很可能是细胞介导的细胞溶解），在致敏细胞与刺激细胞的高比例时占主导；另一种针对反应细胞的特定克隆，在低比例时占主导。
