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 Blood, 1 April 2004, Vol. 103, No. 7, pp. 2691-2698.
Prepublished online as a Blood First Edition Paper on November 26, 2003; DOI 10.1182/blood-2003-09-3184.

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IMMUNOBIOLOGY

CD200 is a novel p53-target gene involved in apoptosis-associated immune tolerance

Michael D. Rosenblum, Edit Olasz, Jeffery E. Woodliff, Bryon D. Johnson, Marja C. Konkol, Kimberly A. Gerber, Rimas J. Orentas, Gordon Sandford, and Robert L. Truitt

From the Department of Pediatrics, Medical College of Wisconsin, Milwaukee; Department of Dermatology, Medical College of Wisconsin, Milwaukee; and Department of Oncology-Cancer Biology, The Johns Hopkins University School of Medicine, Baltimore, MD.

During apoptotic cell death, biochemical processes modify self-proteins and create potential autoantigens. To maintain self-tolerance in the face of natural cell turnover, the immune system must prevent or control responses to apoptosis-associated autoantigens or risk autoimmunity. The molecular mechanisms governing this process remain largely unknown. Here, we show that expression of the immunoregulatory protein CD200 increases as murine dendritic cells (DCs) undergo apoptosis. We define CD200 as a p53-target gene and identify both p53- and caspase-dependent pathways that control CD200 expression during apoptosis. CD200 expression on apoptotic DCs diminishes proinflammatory cytokine production in response to self-antigens in vitro and is required for UVB-mediated tolerance to haptenated self-proteins in vivo. Up-regulation of CD200 may represent a novel mechanism, whereby immune reactivity to apoptosis-associated self-antigens is suppressed under steady state conditions. (Blood. 2004;103: 2691-2698)


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This article has been cited by other articles:


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R. Gorczynski, I. Khatri, L. Lee, and I. Boudakov
An Interaction between CD200 and Monoclonal Antibody Agonists to CD200R2 in Development of Dendritic Cells That Preferentially Induce Populations of CD4+CD25+ T Regulatory Cells
J. Immunol., May 1, 2008; 180(9): 5946 - 5955.
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