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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3457-3464. Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-09-3153.
IMMUNOBIOLOGY T-cell protein tyrosine phosphatase deletion results in progressive systemic inflammatory diseaseFrom the Division of Experimental Medicine, McGill University, Montreal, QC, Canada; Department of Physiology, McGill University, Montreal, QC, Canada; McGill Cancer Centre and Department of Biochemistry, McGill University, Montreal, QC, Canada; and Department of Pathology and Microbiology, University of Nebraska Medical Centre, Omaha, NE.
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-
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| Copyright © 2004 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
. The widespread mononuclear cellular infiltrates correlate with exaggerated interferon-
, 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. (Blood. 2004;103:3457-3464) 
