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J. Biol. Chem., Vol. 278, Issue 9, 7553-7557, February 28, 2003

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Anti-CD95-induced Lethality Requires Radioresistant FcRII⁺ Cells
A NOVEL MECHANISM FOR FULMINANT HEPATIC FAILURE^*

Satoshi Jodo, John T. Kung^§, Sheng Xiao^¶, Derek V. Chan^¶, Seiichi Kobayashi, Masatoshi Tateno^**, Robert Lafyatis, and Shyr-Te Ju^¶§§

From the  Arthritis Center, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, ^§ Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, the ^¶ Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, the  Department of Laboratory Technology, College of Medical Technology, Hokkaido University, Hokkaido, Japan, the ^** Department of Pathology, Sapporo City General Hospital, Sapporo, Japan, and  Division of Rheumatology and Immunology, Department of Internal Medicine, University of Virginia Health System, Charlottesville, Virginia 22908-0412

The Jo2 anti-mouse CD95 monoclonal antibody induces lethality in mice characterized by hepatocyte death and liver hemorrhage. Mice bearing a defect in Fas expression or in the Fas-mediated apoptotic pathway are resistant to Jo2. Here we show that FcRII knockout mice or mice with monoclonal antibody-blocked FcRII are also resistant to Jo2. The critical FcRII⁺ cells are radioresistant and could not be reconstituted with splenic cells. Death of sinusoidal lining cells and destruction of sinusoids were observed, consistent with the characteristic liver hemorrhage and the selective FcRII expression in sinusoidal lining cells but not hepatocytes. Hemorrhage developed coincident with hepatocyte death and the sharp rise of serum alanine aminotransferase and alanine aminotransferase. Invariably, moribund mice showed severe liver hemorrhage and destruction of sinusoids. The data demonstrate a novel mechanism by which the destruction of liver sinusoids, induced by the Jo2-mediated co-engagement of Fas and FcRII, leads to severe hemorrhage and lethal fulminant hepatitis.

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