Bocchieri M H, Riblet R J, Smith J B
Eur J Immunol. 1981 Feb;11(2):159-62. doi: 10.1002/eji.1830110219.
The autologous mixed lymphocyte reaction (AMLR) has been examined in the AMLR-deficient strain, NZB, in C58 mice, which have normal AMLR responses, and in the (NZB x C58) recombinant inbred (NX8 RI) lines. Half of the NX8 RI lines had deficient AMLR and half were comparable in reactivity to the C58 parent strain. AMLR unresponsiveness did not correlate in the NX8 RI lines with H-2 or any other marker known to affect immune recognition. Non-T cells from H-2k NX8 RI lines which had deficient AMLR were able to stimulate an MLR when cultured with T cells of C58 origin. AMLR-positive H-2d lines responded to NZB stimulators, whereas NZB T cells did not respond to any of the H-2d NX8 RI lines but did exhibit strong alloreactivity. Thus, the AMLR defect in NZB mice is due to a T cell lesion. Furthermore, since AMLR deficiency in the NX8 RI lines did not correlate with a positive Coombs test or the production of naturally occurring thymocytotoxic antibody, we conclude that autoimmunity in NZB mice is a complex disease resulting from the inheritance of multiple independently segregating genes.
在AML反应缺陷的品系NZB小鼠、AML反应正常的C58小鼠以及（NZB×C58）重组近交（NX8 RI）系中检测了自体混合淋巴细胞反应（AMLR）。一半的NX8 RI系具有缺陷的AMLR，另一半在反应性上与C58亲本品系相当。在NX8 RI系中，AMLR无反应性与H-2或任何其他已知影响免疫识别的标记物无关。来自具有缺陷AMLR的H-2k NX8 RI系的非T细胞与C58来源的T细胞一起培养时能够刺激混合淋巴细胞反应（MLR）。AMLR阳性的H-2d系对NZB刺激物有反应，而NZB T细胞对任何H-2d NX8 RI系均无反应，但表现出强烈的同种异体反应性。因此，NZB小鼠中的AMLR缺陷是由于T细胞损伤所致。此外，由于NX8 RI系中的AMLR缺陷与抗人球蛋白试验阳性或天然存在的胸腺细胞毒性抗体的产生无关，我们得出结论，NZB小鼠中的自身免疫是一种复杂的疾病，由多个独立分离基因的遗传导致。
