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(Circulation. 2006;114:1901-1904.)
© 2006 American Heart Association, Inc.

Editorial

Immunosuppression in Atherosclerosis

Mobilizing the Opposition Within

Jörg J. Goronzy, MD; Cornelia M. Weyand, MD

From the Kathleen B. and Mason I. Lowance Center for Human Immunology, Emory University School of Medicine, Atlanta, Ga.

Correspondence to Dr Cornelia M. Weyand, Lowance Center for Human Immunology, 101 Woodruff Circle, Atlanta, GA 30322. E-mail cweyand@emory.edu

Key Words: Editorials • atherosclerosis • immune system • inflammation • lymphocytes • plaque • T-lymphocytes, regulatory

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

An estimated 10¹⁴ microbes live on our mucosal surfaces, exceeding by far the number of cells in our body (approximately 10¹³). Survival depends on our ability to recognize, wall off, and eliminate unwanted intruders. The doubling of life expectancy over the last century has created an internal burden of degenerating tissue, cellular debris, and malignant transformation, adding considerable stress to host defense mechanisms. The most powerful protective tool that we have is inflammation, a generic response pattern that allows the immune system to rapidly recognize threats, mobilize cells to injury sites, remove instigators, and heal wounds.

Articles pp 1968 and 1977

Acute inflammation is short-lived and characterized by the recruitment of polymorphonuclear granulocytes followed by monocytes. Inflammation is self-amplifying and intensified through the sequential release of lipid mediators, cytokines, and chemokines. By 48 to 72 hours, granulocytes are replaced by lymphocytes. Despite the domino effect of a few inflammatory cells recruiting millions of others, inflammation is usually self-limited, resolving within days to weeks. If not, the response switches to chronic mode. Lymphocytes then dominate the force of inflammatory cells, and new rules dictate cell-cell communication, collateral damage, and repair. Most diseases categorized as chronic inflammatory disorders persist over decades, bringing a much greater time dimension to the inflammatory process. Although atherosclerosis is a quintessential chronic, persistent inflammatory disease,¹ it differs from most others because its smoldering disease activity lasts for 30 to 70 years.

Obviously, the mechanisms of acute and chronic inflammation are distinct; granulocytes and lymphocytes utilize fundamentally . . . [Full Text of this Article]

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Issue Highlights
Circulation 2006 114: 1897. [Extract] [Full Text]