The other side of immunoglobulin G: suppressor of inflammation

被引：62

作者：

Aschermann, S. ^{[1
]}

Lux, A. ^{[1
]}

Baerenwaldt, A. ^{[1
]}

Biburger, M. ^{[1
]}

Nimmerjahn, F. ^{[1
]}

机构：

[1] Univ Erlangen Nurnberg, Dept Med 3, Nikolaus Fiebiger Ctr Mol Med, Lab Expt Immunol & Immunotherapy, D-91054 Erlangen, Germany

来源：

CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 2010年 / 160卷 / 02期

关键词：

Fc receptors; glycosylation; immunoglobulin G; inflammation; IVIG; IMMUNE THROMBOCYTOPENIC PURPURA; FC-GAMMA RECEPTORS; T-CELL LEUKEMIA; INTRAVENOUS IMMUNOGLOBULIN; ANTIINFLAMMATORY ACTIVITY; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY; AUTOIMMUNE-DISEASE; DEFICIENT MICE; MURINE MODEL;

D O I：

10.1111/j.1365-2249.2009.04081.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

P>Immunoglobulin G (IgG) molecules can have two completely opposite functions. On one hand, they induce proinflammatory responses and recruit innate immune effector cells during infection with pathogenic microorganisms or autoimmune disease. On the other hand, intravenous infusion of high doses of pooled IgG molecules from thousands of donors [intravenous IG (IVIG) therapy] represents an efficient anti-inflammatory treatment for many autoimmune diseases. Whereas our understanding of the mechanism of the proinflammatory activity of IgG is quite advanced, we are only at the very beginning to comprehend how the anti-inflammatory activity comes about and what cellular and molecular players are involved in this activity. This review will summarize our current knowledge and focus upon the two major models of either IVIG-mediated competition for IgG-triggered effector functions or IVIG-mediated adjustment of cellular activation thresholds used to explain the mechanism of the anti-inflammatory activity.

引用

页码：161 / 167

页数：7

共 51 条

[1] The MHC class I-like Fc receptor promotes humorally mediated autoimmune disease [J].