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(Circulation Research. 2006;98:e26.)
© 2006 American Heart Association, Inc.

Letter to the Editor

FcIIB and Cardiovascular Inflammatory Disease

Chiharu Kishimoto, Keisuke Shioji, Zuyi Yuan

Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with great interest the article by Mineo and colleagues¹ exploring the role of FcIIB, an inhibitory receptor of FcIIs, on C-reactive protein (CRP)-mediated endothelial dysfunction. Mineo et al examined the mechanisms of CRP actions on endothelium by testing the hypothesis that CRP attenuates endothelial NO synthase (eNOS) activation in vitro. The investigators found that CRP-induced declines in NO production promote monocyte adhesion to endothelium. They further investigated the role of Fc receptors, which display high affinity for CRP and modulate CRP actions. They found that, in FcRIIB^+/+ mice, CRP blunts acetylcholine-induced increases in carotid artery vascular conductance, and that, in contrast, CRP enhances acetylcholine responses in FcRIIB^–/– mice. They concluded that FcRIIB mediates CRP inhibition of eNOS.

At first glance, their results appear to be contradictory to previous reports by our own group^2,3 and by Gill et al.⁴ In our study, not only FcRIIB-mediated inhibitory effect on experimental autoimmune myocarditis in rats² but FcRIIB-mediated antiatherosclerotic effect in apolipoprotein E–deficient mice³ were demonstrated, using immunoglobulin preparations. Gill et al⁴ demonstrated the targeting effect of immunoglobulin on adhesion molecules using ischemia–reperfusion model in cats, suggesting the downregulation of adhesion molecules via Fc receptors.

The fact that FcRIIB mediates CRP inhibition of eNOS, resulting in endothelial dysfunction, is not necessarily in contradiction to aforementioned studies from different groups.^2–4 The precise effect of FcRIIB on cardiovascular inflammatory cascades may depend on experimental models. Such opposite activatory and inhibitory actions of . . . [Full Text of this Article]