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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:17.)
© 2005 American Heart Association, Inc.

Brief Reviews

ATVB In Focus

Immunity and Atherosclerosis

Göran K. Hansson

From the Center for Molecular Medicine and Department of Medicine, Karolinska University Hospital, Stockholm, Sweden.

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

In the last two years, the concept that atherosclerosis is an inflammatory disease has moved from the scientific journals to the lay press and TV programs. Family physicians are as interested as vascular biologists in inflammatory mechanisms of the vessel wall. CRP is used to screen for and monitor coronary heart disease patients, and antiinflammatory strategies are being developed as targets for cardiovascular therapy.

See page 18

Inflammation is an effector mechanism of the immune system. It is elicited after activation of immunity through the adaptive and/or innate pathways. While the former depends on antigen recognition by T and B cells, the latter pathway is activated when pathogen-associated molecular patterns ligate pattern recognition receptors on several cell types, including macrophages and endothelial cells. Innate immunity does not depend on clonal expansion and therefore mounts rapid responses to invading microorganisms. As a drawback, it relies on recognition of molecular patterns that are shared by microbial molecules (eg, endotoxins and heat shock proteins) but which may also appear on endogenous ones. In contrast, adaptive immunity is highly specific, with millions of T and B cell receptors generated through somatic rearrangements of T cell receptors and Ig genes. This makes for a remarkable degree of fine specificity in the adaptive immune response. The price for this high degree of specificity is loss of speed. Each unique receptor is present on only one or a few cells; specific cells therefore have to multiply repeatedly before effector responses of sufficient magnitudes can be mounted. These . . . [Full Text of this Article]

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