LFA-3, CD44, AND CD45--PHYSIOLOGIC TRIGGERS OF MONOCYTE TNF AND IL-1 RELEASE

我们以前曾报道，连接三个单核细胞表面 抗原通过其特异性固定化抗体，诱导 来自人单核细胞的IL-1和TNF。 这项工作的结果是 发表于Science 249：1295-97，1990。 我们目前正在调查 这些表面抗原之一，CD 44，是否参与了 内毒素对人单核细胞的作用。 我们观察到， 加入内毒素的人单核细胞，表达CD 44，但不 其他几种表面抗原，降低了约25%。 在 此外，我们还发现了一种抗CD 44抗体，它能够阻断 内毒素诱导单核细胞释放TNF。这种TNF的抑制作用 释放可能是抗体和抗体之间竞争性结合的结果。 内毒素 为了确定CD 44是否是一种结合蛋白， 内毒素，我们计划使用放射性标记的 内毒素 然后我们将确定受体-内毒素复合物是否能 被CD 44抗体免疫沉淀。

We have previously reported that the ligation of three monocyte surface antigens, by their specific immobilized antibodies, induces the release of IL-1 and TNF from human monocytes. The results of this work were published in Science 249:1295-97, 1990. We are currently investigating whether one of these surface antigens, CD44, is involved in the binding of endotoxin to human monocytes. We have observed that one hour after the addition of endotoxin to human monocytes, the expression of CD44, but not several other surface antigens, is lowered by approximately 25%. In addition, we have found an anti-CD44 antibody which is able to block the endotoxin induced TNF release from monocytes. This inhibition of TNF release may be the result of competitive binding between the antibody and endotoxin. To determine if CD44 is one of the binding proteins for endotoxin, we plan to carry out crosslinking studies using radiolabeled endotoxin. We will then determine if the receptor-endotoxin complexes can be immunoprecipitated by antibodies to CD44.