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(Circulation Research. 2006;99:1154.)
© 2006 American Heart Association, Inc.

Editorials

A Novel Approach to the Suppression of Atherosclerosis by Fc Receptor Blockade

Chiharu Kishimoto

From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Japan.

Correspondence to Chiharu Kishimoto, MD, PhD, Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, 54 Kawaracho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. E-mail kkishi@kuhp.kyoto-u.ac.

See related article, pages 1188–1196

Key Words: Fc receptors • atherosclerosis • myocarditis • immunoglobulin

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

	Introduction

 
A therosclerosis is associated with immune activation and with systemic immune responses and signs of inflammation.^1–3 Atherosclerotic plaques contain a large number of immune cells, particularly macrophages and T cells.^4,5 Histopathological and clinical investigations point to immune activation of plaques as a cause of plaque rupture and acute coronary syndromes. Seroepidemiological studies suggest links between atherosclerosis and microbial infections.^6,7 Animal studies have identified specific immune cells that play a role in atherogenesis. For example, congenital deficiency of macrophages, lymphocytes, and the Th₁ effector pathway, generated by cross-breeding apolipoprotein (apo) E knockout (KO) mice with op/op mutant mice,⁸ recombinase acting gene-1 KO mice,⁹ and interferon- receptor KO mice,¹⁰ respectively, have resulted in the reduction of aherosclerotic lesions. Furthermore, the blockade of c-fms, a receptor for macrophage colony stimulating factor, also caused marked suppression of atherogenesis in apo E-deficient mice, where macrophage differentiation was impaired. These and other studies suggest that immunomodulation may be used to treat or prevent atherosclerosis.

Therapy with immunoglobulin has been used in the treatment of immune-mediated disorders for more than 25 years.^11–13 The mode of action of immunoglobulin is still unclear and may involve both Fc and V region-dependent mechanisms: blockade of Fc receptors on macrophages and effector cells, antiinflammatory effects by attenuation of complement-mediated damage, regulation of the production of cytokines, or inhibition of lymphocyte proliferation. Several of these mechanisms might be beneficial in atherosclerosis.¹⁴ Indeed, we have found that immunoglobulin therapy markedly suppressed atherosclerosis because of Fc receptor-mediated immunomodulatory actions in apoE-deficient mice.¹⁵

In . . . [Full Text of this Article]

Related Article:

Fc Receptor Deficiency Confers Protection Against Atherosclerosis in Apolipoprotein E Knockout Mice

Purificación Hernández-Vargas, Guadalupe Ortiz-Muñoz, Oscar López-Franco, Yusuke Suzuki, Julio Gallego-Delgado, Guillermo Sanjuán, Alberto Lázaro, Virginia López-Parra, Luis Ortega, Jesús Egido, and Carmen Gómez-Guerrero
Circ. Res. 2006 99: 1188-1196. [Abstract] [Full Text] [PDF]