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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.

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IMMUNOBIOLOGY

T-cell protein tyrosine phosphatase deletion results in progressive systemic inflammatory disease

Krista M. Heinonen, Frederick P. Nestel, Evan W. Newell, Gabrielle Charette, Thomas A. Seemayer, Michel L. Tremblay, and Wayne S. Lapp

From 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-{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. (Blood. 2004;103:3457-3464)


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