© 1999 American Heart Association, Inc.
Editorial |
IL-10: An "Immunologic Scalpel" for Atherosclerosis?
From the San Diego VA Medical Center, University of California San Diego.
Correspondence to Robert A. Terkeltaub, MD, Chief, Rheumatology Section, San Diego VA Medical Center, Professor of Medicine in Residence, University of California San Diego, 3350 La Jolla Village Dr (111K), San Diego, CA 92161. E-mail rterkeltaub@ucsd.edu
Key Words: atherosclerosis • interleukin-10 • MM-LDL • monocytes
Mononuclear leukocyte–mediated inflammation is a central feature of atherosclerosis. Using measures that diminish lesion monocyte recruitment and macrophage-mediated inflammation, investigators have shown these specific events to be essential to the development and progression of atherosclerotic lesions. Lesion T lymphocytes have an activated phenotype and colocalize with lesion macrophages, particularly in early disease. However, the role of lesion T lymphocytes in atherogenesis is not as well understood as the role of macrophages.
A variety of inflammatory mediators, including cytokines,
growth factors, and proinflammatory lipids, are present in
atherosclerotic lesions. However, even in the complex milieu of a
chronic inflammatory locus, a limited number of cytokines can
become dominant. This concept has most recently been illustrated by the
dramatic success of inhibitors of tumor necrosis factor
(TNF)-
in the treatment of rheumatoid arthritis. Thus, certain
inhibitors of cytokines, or anti-inflammatory
cytokines, have been proposed as potential "immunologic
scalpels" to diminish the activity of several chronic mononuclear
leukocyte–mediated inflammatory diseases.
Interleukin (IL)-10, a prototypical anti-inflammatory cytokine, is under investigation (and in a few cases at the stage of clinical trials) for therapy of a variety of chronic diseases. These include rheumatoid arthritis, inflammatory bowel disease, psoriasis, multiple sclerosis, allergic eosinophilic inflammation, Wegener’s granulomatosis, and cardiac allograft rejection. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology,1 Pinderski Oslund et al present a novel chapter in an evolving story on the potential modulatory role of IL-10 in atherosclerosis.
A cross-regulatory role in atherosclerosis of the
activated monocyte-macrophage (and Th2 immune response)
product IL-10
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