Submitted on February 29, 2008
Revised on June 18, 2008
Roles of Heat Shock Proteins and 
T cells in Inflammation
Mark I Hirsh1 and Wolfgang G Junger1*
1 Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: wjunger{at}bidmc.harvard.edu.
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 towards macrophages and neutrophils that express Hsp60 and Hsp70, respectively, protecting host organs from collateral tissue damage by phagocytes.
