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Review Article
Mechanisms of Disease
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Volume 353:1711-1723 October 20, 2005 Number 16
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Antiinflammatory Action of Glucocorticoids — New Mechanisms for Old Drugs
Turk Rhen, Ph.D., and John A. Cidlowski, Ph.D.

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Inflammation is a reflexive response to infection, the binding of antibodies to antigens within the body, mechanical irritation, or injury.1 Microbes that breach epithelial barriers, for instance, directly activate complement and toll-like receptors, two principal components of the innate immune system. The activation of these sentinels triggers the synthesis and release of inflammatory mediators with acute effects on the vasculature. Localized vasodilation, increased vascular permeability, extravasation of plasma (and humoral) proteins, and migration of leukocytes into the affected tissue produce the classic signs of inflammation: calor, dolor, rubor, tumor, and functio laesa. A positive feedback loop initiates the production of . . . [Full Text of this Article]

Basic Actions of Endogenous Glucocorticoids

Structure of the Glucocorticoid Receptor

Post-Translational Modifications of the Glucocorticoid Receptor

Neuroendocrine Regulation of Inflammation

Antiinflammatory Signaling Mechanisms

Limitations of Glucocorticoid Therapy

Selective Glucocorticoids and Future Therapy

Conclusions


Source Information

From the Department of Biology, University of North Dakota, Grand Forks (T.R.); the Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, N.C. (J.A.C.); and the Department of Health and Human Services, National Institutes of Health, Bethesda, Md. (J.A.C.).

Address reprint requests to Dr. Cidlowski at the Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, 111 T.W. Alexander Dr., Research Triangle Park, NC 27709, or at cidlows1@niehs.nih.gov.


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