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Roles of Heat Shock Proteins and T Cells in Inflammation

¹ Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts

Correspondence and requests for reprints should be addressed to Wolfgang G. Junger, Ph.D., Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Ave., E/ST-8M10C, Boston, MA 02215. E-mail: wjunger{at}bidmc.harvard.edu

Abstract

Elimination of activated inflammatory cells that infiltrate and damage host organs can reduce morbidity and mortality. A better understanding of the mechanisms by which these processes occur may lead to new approaches to prevent tissue damage. The lungs, gastrointestinal tract, and skin are particularly prone to infection and collateral damage by inflammatory cells. Specialized lymphocytes protect these organs from collateral tissue damage by eliminating neutrophils and macrophages from inflamed tissues. These lymphocytes recognize signals produced by inflammatory cells. One such signal is heat shock protein (Hsp) expressed on the cell surface of inflamed phagocytes. Mammalian Hsp molecules closely resemble their microbial equivalents, and therefore phagocytes decorated with these molecules are recognized as target cells. T lymphocytes bearing the T cell receptor (TCR) elicit cytotoxic activity toward macrophages and neutrophils that express Hsp60 and Hsp70, respectively, protecting host organs from collateral tissue damage by phagocytes.

Key Words: TCR • macrophages • neutrophils • inflammatory tissue damage • immunoregulation

CLINICAL RELEVANCE This review describes the role of heat shock proteins in target cell removal by the immune surveillance system in the context of inflammatory diseases and cancer. Special emphasis is on the resolution of inflammation from the lungs.