Inflammation is a reflexive response to infection, the bindingof 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 principalcomponents of the innate immune system. The activation of thesesentinels triggers the synthesis and release of inflammatorymediators with acute effects on the vasculature. Localized vasodilation,increased vascular permeability, extravasation of plasma (andhumoral) proteins, and migration of leukocytes into the affectedtissue produce the classic signs of inflammation: calor, dolor,rubor, tumor, and functio laesa. A positive feedback loop initiatesthe 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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