T-cell protein tyrosine phosphatase deletion results in progressive systemic inflammatory disease
摘要：
The deregulation of the immune response is a critical component in inflammatory disease. Recent in vitro data show that T-cell protein tyrosine phosphatase (TC-PTP) is a negative regulator of cytokine signaling. Furthermore, tc-ptp(-/-) mice display immune defects and die within 5 weeks of birth. We report here that tc-ptp(-/-) mice develop progressive systemic inflammatory disease as shown by chronic myocarditis, gastritis, nephritis, and sialadenitis as well as elevated serum interferon-gamma. The widespread mononuclear cellular infiltrates correlate with exaggerated interferon-gamma, tumor necrosis factor-alpha, interleukin-12, and nitric oxide production in vivo. Macrophages grown from tc-ptp(-/-) mice are inherently hypersensitive to lipopolysaccharide, which can also be detected in vivo as an increased susceptibility to endotoxic shock. These results identify T-cell protein tyrosine phosphatase as a key modulator of inflammatory signals and macrophage function.
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关键词：
Animals Mice, Knockout Mice T-Lymphocytes Macrophages Cells, Cultured Shock, Septic Inflammation Inflammation Mediators Up-Regulation
DOI：
10.1182/blood-2003-09-3153
被引量：
年份：
2004
Elsevier
Semantic Scholar
Semantic Scholar
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万方医学
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NCBI
NCBI
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ResearchGate
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bloodjournal.org
bloodjournal.org
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onAcademic
bloodjournal.hematologylibrary.org
frontiersin.org
circgenetics.ahajournals.org
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