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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. This Article Full Text (PDF) All Versions of this Article: 2003-09-3153v1 103/9/3457    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Heinonen, K. M Articles by Lapp, W. S Search for Related Content PubMed PubMed Citation Articles by Heinonen, K. M Articles by Lapp, W. S Social Bookmarking                   What's this? Submitted September 15, 2003 Accepted January 4, 2004 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* Division of Experimental Medicine, McGill University, Montreal, Quebec, Canada; Department of Physiology, McGill University, Montreal, Quebec, Canada; McGill Cancer Centre, McGill University, Montreal, Quebec, Canada Department of Physiology, McGill University, Montreal, Quebec, Canada Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA McGill Cancer Centre, McGill University, Montreal, Quebec, Canada; Department of Biochemistry, McGill University, Montreal, Quebec, Canada Department of Physiology, McGill University, Montreal, Quebec, Canada; Division of Experimental Medicine, McGill University, Montreal, Quebec, Canada * Corresponding author; email: wayne.lapp{at}mcgill.ca. 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 five 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-. The widespread mononuclear cellular infiltrates correlate with exaggerated interferon-, tumor necrosis factor-, 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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