INFLAMMATORY MEDIATOR RELEASE FROM HUMAN MONOCYTES VIA IMMOBILIZED FC-RECEPTORS - ITS POTENTIAL ROLE IN ADVERSE REACTIONS TO SYSTEMIC MONOCLONAL-ANTIBODY THERAPY

被引：13

作者：

HOFFMAN, T

TRIPATHI, AK

LEE, YL

BONVINI, E

GOLDING, B

机构：

[1] Laboratory of Cell Biology, Division of Hematology, Center for Biologies Evaluation and Research

[2] Food and Drug Administration, Bethesda, MD

[3] HFB-450, Bethesda, MD, 20892, Building 29

来源：

TRANSPLANTATION | 1992年 / 54卷 / 02期

关键词：

D O I：

10.1097/00007890-199208000-00027

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Human monocytes released superoxide anion, IL-1, and TNF subsequent to binding of their Fc receptor I to murine IgG2a or rabbit IgG. Fc receptor II binding to murine IgG2b or IgG1 had similar consequences. Immobilized murine monoclonal antibodies, IgG2a anti-CD3 (OKT3) or IgG1 anti-CD44 also induced superoxide anion and monokine production. Monocytes bound OKT3 via FcRI and responded to immobilized OKT3 by inflammatory mediator release in the absence of T cells. These results suggest that direct interaction of immunoglobulins with monocytes via FcR may represent an important phase of the pathophysiology of adverse reactions to systemic monoclonal antibodies.

引用

页码：343 / 346

页数：4

共 16 条

[1]

Abrahamsen T G, 1991, J Clin Apher, V6, P48, DOI 10.1002/jca.2920060110

[2] INVIVO CELL ACTIVATION FOLLOWING OKT3 ADMINISTRATION - SYSTEMIC CYTOKINE RELEASE AND MODULATION BY CORTICOSTEROIDS [J].