Aschermann S, Lux A, Bärenwaldt A, Biburger M, Nimmerjahn F (2010)
Publication Status: Published
Publication Type: Journal article, Review article
Publication year: 2010
Publisher: Wiley-Blackwell
Book Volume: 160
Pages Range: 161-167
Journal Issue: 2
DOI: 10.1111/j.1365-2249.2009.04081.x
Summary 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. © 2009 British Society for Immunology.
APA:
Aschermann, S., Lux, A., Bärenwaldt, A., Biburger, M., & Nimmerjahn, F. (2010). The other side of immunoglobulin G: Suppressor of inflammation. Clinical and Experimental Immunology, 160(2), 161-167. https://doi.org/10.1111/j.1365-2249.2009.04081.x
MLA:
Aschermann, Susanne, et al. "The other side of immunoglobulin G: Suppressor of inflammation." Clinical and Experimental Immunology 160.2 (2010): 161-167.
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