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肺炎球菌诱导人血小板释放血清素。确定参与的血浆/血清因子为免疫球蛋白。

Pneumococcus-induced serotonin release from human platelets. Identification of the participating plasma/serum factor as immunoglobulin.

作者信息

Zimmerman T S, Spiegelberg H L

出版信息

J Clin Invest. 1975 Oct;56(4):828-34. doi: 10.1172/JCI108161.

Abstract

Pneumococcus-induced serotonin release from human platelets is greatly facilitated by a factor present in normal human plasma and serum. We have identified this factor as immunoglobulin by: (a) removing if from plasma and serum with solid phase antiFab antibody; (b) demonstrating its absence from the serum of an individual with severe immunoglobulin deficiency; and, (c) showing its presence in IgG preparations isolated from normal individuals. Evidence suggesting that the release reaction is triggered by pneumococcal antigen-antibody complexes rather than by nonimmune interaction of immunoglobulin with pneumococcus includes: (a) the failure of isolated IgG myeloma proteins to support release; (b) a lack of correlation between IgG concentration and "releasing factor activity" in normal human sera; (c) the identification of a normal serum that supports release by types II and III pneumococci but not type VII; and, (d) the ability of most normal sera to support release by pneumococca serotypes II and VII, though these types have not shown nonimmune reactivity with the Fc portion of the IgG molecule. The ability of antibodies present in normal serum to support pneumococcus-induced serotonin release suggests that the thrombocytopenia seen in pneumococcal infection may at least in part be caused by pneumococcal antigen-antibody complexes.

摘要

正常人体血浆和血清中的一种因子可极大促进肺炎球菌诱导的人血小板释放血清素。我们已通过以下方式将该因子鉴定为免疫球蛋白:(a) 用固相抗Fab抗体从血浆和血清中去除该因子;(b) 证明严重免疫球蛋白缺乏个体的血清中不存在该因子;以及 (c) 显示从正常个体分离的IgG制剂中存在该因子。表明释放反应由肺炎球菌抗原 - 抗体复合物而非免疫球蛋白与肺炎球菌的非免疫相互作用触发的证据包括:(a) 分离的IgG骨髓瘤蛋白无法支持释放;(b) 正常人血清中IgG浓度与“释放因子活性”之间缺乏相关性;(c) 鉴定出一种正常血清,其支持II型和III型肺炎球菌释放但不支持VII型;以及 (d) 大多数正常血清支持肺炎球菌血清型II和VII释放的能力,尽管这些血清型未显示与IgG分子Fc部分的非免疫反应性。正常血清中存在的抗体支持肺炎球菌诱导的血清素释放的能力表明,肺炎球菌感染中出现的血小板减少症可能至少部分是由肺炎球菌抗原 - 抗体复合物引起的。

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