作者: Mark I. Hirsh , Wolfgang G. Junger
DOI: 10.1007/978-1-4020-5585-0_21
关键词: Inflammation 、 Immune system 、 Heat shock protein 、 Cell 、 T-cell receptor 、 Chemistry 、 HSP60 、 Cell biology 、 Cytotoxic T cell 、 Hsp70
摘要: Depletion of phagocytes that infiltrate host organs like the lungs reduces inflammatory damage to tissues. Understanding mechanisms by which this process occurs could lead new therapeutic approaches limit detrimental effects inflammation. The lungs, gastrointestinal tract, and skin are particularly prone infection. Specialized immune cells protect these from tissue eliminating inflamed tissues recognizing signals produced phagocytes. One such signal is heat shock proteins (HSP) expressed on cell surface These HSP closely resemble their microbial equivalents, therefore labeled recognized as target cells. T lymphocytes bearing γδT receptor (TCR) elicit fast responses invading pathogens. Since γδTCR has limited germline-encoded diversity, an ideal for recognition exert cytotoxic actions towards macrophages neutrophils express Hsp60 or Hsp70, respectively, surface. Through cells, eliminate sites, thereby preventing