Heat Shock Proteins and the Resolution of Inflammation by Lymphocytes

Depletion of phagocytes that infiltrate host organs like the lungs reduces inflammatory damage to tissues. Understanding the mechanisms by which this process occurs could lead to new therapeutic approaches to limit the detrimental effects of inflammation. The lungs, gastrointestinal tract, and skin are particularly prone to infection. Specialized immune cells protect these organs from tissue damage by eliminating phagocytes from inflamed tissues by recognizing signals produced by the phagocytes. One such signal is heat shock proteins (HSP) expressed on the cell surface of phagocytes. These HSP closely resemble their microbial equivalents, and therefore phagocytes that are labeled by HSP are recognized as target cells. T lymphocytes bearing γδT cell receptor (TCR) elicit fast responses to invading pathogens. Since the γδTCR has limited germline-encoded diversity, HSP are an ideal target for recognition by these cells. γδT cells exert cytotoxic actions towards macrophages and neutrophils that express Hsp60 or Hsp70, respectively, on their cell surface. Through the recognition of HSP on the cell surface of inflamed cells, γδT cells eliminate phagocytes from inflammatory sites, thereby preventing host tissue damage