Zuberi R I, Katz D H
Cell Immunol. 1984 Apr 1;84(2):299-310. doi: 10.1016/0008-8749(84)90101-1.
The present studies were undertaken to define the contribution of the autologous or syngeneic mixed-leukocyte reactions (AMLR/SMLR) to the cellular proliferation observed in unfractionated spleen cell cultures. Proliferation was studied in whole, untreated 6-day murine spleen cell cultures supplemented with syngeneic serum. These cultures exhibited relatively low but significant levels of cellular proliferation as measured by uptake of radioactive thymidine ([3H]TdR). Treatment of spleen cells with monoclonal anti-Thy 1.2 antibody and complement before culture, the addition of specific anti-I-A monoclonal antibodies to the cultures or removal of Ia+ adherent cells before initiation of culture all inhibited the proliferative response significantly. Thus, the autologous proliferation of untreated and unfractionated spleen cells manifests the main characteristics of the AMLR/SMLR, namely, its dependence on T (responder) and Ia+ (stimulator) cells and specific inhibition by anti-I-A antibodies. A marked augmentation in cellular proliferation was observed in unfractionated spleen cell cultures treated for the initial 24 hr of culture with 5 X 10(-6) M indomethacin, an inhibitor of prostaglandin synthesis. Conversely, the addition of 7 X 10(-9) M prostaglandin E1 (PGE1) to these cultures depressed cellular proliferation. This suppression of autologous splenic cell proliferation induced by PGE1 could be partially reversed by the addition of concanavalin A-induced lymphokine (LK) preparations early in the culture. These findings indicate that (a) the proliferation of unfractionated spleen cell cultures occurring in the absence of exogenous stimulatory signals is due largely to an ongoing AMLR, and (b) biologically active mediators with opposing influences, namely, prostaglandins and immunostimulatory LK, participate in the regulation of the AMLR.
开展本研究以明确自体或同基因混合淋巴细胞反应（AMLR/SMLR）对未分级脾细胞培养物中观察到的细胞增殖的作用。在添加同基因血清的完整、未处理的6日龄小鼠脾细胞培养物中研究增殖情况。通过放射性胸苷（[3H]TdR）摄取量测定，这些培养物表现出相对较低但显著的细胞增殖水平。在培养前用单克隆抗Thy 1.2抗体和补体处理脾细胞、向培养物中添加特异性抗I-A单克隆抗体或在培养开始前去除Ia+黏附细胞，均显著抑制增殖反应。因此，未处理和未分级脾细胞的自体增殖体现了AMLR/SMLR的主要特征，即其对T（反应细胞）和Ia+（刺激细胞）的依赖性以及抗I-A抗体的特异性抑制作用。在用5×10(-6) M吲哚美辛（一种前列腺素合成抑制剂）处理培养最初24小时的未分级脾细胞培养物中，观察到细胞增殖显著增强。相反，向这些培养物中添加7×10(-9) M前列腺素E1（PGE1）可抑制细胞增殖。在培养早期添加刀豆球蛋白A诱导的淋巴因子（LK）制剂可部分逆转PGE1诱导的自体脾细胞增殖抑制。这些发现表明：（a）在无外源性刺激信号情况下发生的未分级脾细胞培养物增殖在很大程度上归因于持续存在的AMLR；（b）具有相反作用的生物活性介质，即前列腺素和免疫刺激LK，参与AMLR的调节。
