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37. Heat Shock Proteins and the Resolution of Inflammation by Lymphocytes.

Author

Asea, A. A. A., Calderwood, S. K., Asea, Alexzander A. A., Maio, Antonio De, Hirsh, Mark I., and Junger, Wolfgang G.

Abstract

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 [ABSTRACT FROM AUTHOR]

Published
2007
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50. Autocrine regulation of T-cell activation by ATP release and P2X7 receptors.

Author

Yip, Linda, Woehrle, Tobias, Corriden, Ross, Hirsh, Mark, Yu Chen, Inoue, Yoshiaki, Ferrari, Vhe, Insel, Paul A., and Junger, Wolfgang G.

Subjects
AUTOCRINE mechanisms, T cells, ADENOSINE triphosphate, CALCIUM in the body, GENE expression, LYMPHOCYTES
Abstract

T-cell activation requires the influx of extracellular calcium, although mechanistic details regarding such activation are not fully defined. Here, we show that P2X7 receptors play a key role in calcium influx and downstream signaling events associated with the activation of T cells. By real-time PCR and immunohistochemistry, we find that Jurkat T cells and human 4+ CD T cells express abundant P2X7 receptors. We show, using a novel fluorescent microscopy technique, that T-cell receptor (TCR) stimulation triggers the rapid release of ATP (< 100 µM). This release of ATP is required for TCR-mediated calcium influx, NFAT activation, and interleukin-2 (IL-2) production. TCR activation up-regulates P2X7 receptor gene expression. Removal of extracellular ATP by apyrase or alkaline phosphatase treatment, inhibition of ATP release with the maxi-anion channel blocker gadolinium chloride, or siRNA silencing of P2X7 receptors blocks calcium entry and inhibits T-cell activation. Moreover, lymphocyte activation is impaired in C57BL/6 mice that express poorly functional P2X7 receptors, compared to control BALB/c mice, which express fully functional P2X7 receptors. We conclude that ATP release and autocrine, positive feedback through P2X7 receptors is required for the effective activation of T cells. [ABSTRACT FROM AUTHOR]

Published
2009
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