CROSS LINKING OF CLASS II MOLECULES AS A SIGNAL IN SPECIFIC MONOCYTE REGULATION

人淘析器纯化的单核细胞与抗HLA-DR或DQ的孵育 抗体可抑制血清诱导的花生四烯酸释放 酵母聚糖（STZ）是一种吞噬刺激物，已知其诱导肌醇 磷脂水解和Ca（+2）内流。然而，只有抗HLA-DR 抗体部分抑制STZ诱导的磷酸肌醇水解， 伴刀豆球蛋白A诱导的Ca（+2）内流。用抗HLA-DR或DQ孵育 抗体抑制佛波酯诱导的AA释放以及超氧化物 生产和IL-1释放。抗类对单核细胞功能的抑制 II抗体不伴随cAMP升高。此外，除了 外源性db-cAMP和其他药物（毛喉素、霍乱毒素或IBMX） 可以通过不同的机制增加cAMP水平，单独或联合 与抗HLA抗体结合，对因子 release.我们的结果表明，第二类分子的微扰 在信号的多个点下调细胞激活 磷酸肌醇远端显性抑制的转导途径 水解他们还表明，抗HLA II类抗体的抑制作用 抗体可能不是通过cAMP升高介导的。

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 accompanied by cAMP elevation. Furthermore, addition of exogenous db-cAMP and other agents (forskolin, cholera toxin, or IBMX) 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.