CROSS LINKING OF CLASS II MOLECULES AS A SIGNAL IN REGULATION OF MONOCYTES

洗脱剂纯化的单核细胞与抗人类白细胞抗原DR或DQ的孵育 抗体抑制血清诱导的花生四烯酸释放 处理过的酵母多糖(STZ)，一种已知的诱导 肌醇磷脂水解和Ca+2内流。然而，只有反- HLA-DR抗体部分抑制链脲佐菌素诱导的磷酸肌醇 水解和刀豆蛋白A诱导的Ca+2内流。孵化与 抗人类白细胞抗原DR或DQ抗体抑制佛波酯诱导的AA释放 以及超氧化物歧化和IL-1的释放。抑制单核细胞 抗II类抗体的作用与cAMP无关 立面。此外，这可以通过不同的方式提高cAMP水平 机制，单独或与抗人类白细胞抗原抗体结合，没有 对因子释放的抑制作用。我们的结果表明， II类分子的扰动下调了细胞的激活 多个信号转导途径中的一个以上具有显性 抑制肌醇磷酸水解酶的远端。他们还建议 抗人类白细胞抗原II类抗体的抑制作用可能不是 通过营地提升来调停。

Incubation of human elutriator-purified monocytes with anti-HLA-DR or DQ antibody inhibited the release of arachidonic acid induced by serum- treated zymosan (STZ), a phagocytic stimulus which is known to induce inositol phospholipid hydrolysis and Ca+2 influx. However, only anti- HLA-DR antibody partially inhibited STZ-induced inositol phosphate hydrolysis and concanavalin-A-induced Ca+2 influx. Incubation with anti-HLA-DR or DQ antibody inhibited phorbol ester-induced AA release as well as superoxide production and IL-1 release. Inhibition of monocyte function by anti-class II antibodies was not accompained by cAMP elevation. Furthermore, that can increase cAMP levels through different mechanisms, alone or in combination with anti-HLA antibodies, had no inhibitory effect on factor release. Our results demonstrate that perturbation of class II molecules down modulates cell activation at more than one point of the signal transduction pathway with dominant inhibition distal to inositol phosphate hydrolysis. They also suggest that the inhibition by anti-HLA Class II antibody is probably not mediated via cAMP elevation.