Human leukocyte antigen class I-independent pathways may contribute to hepatitis B virus-induced liver disease after liver transplantation

Authors

  • Gabriele Missale,

    1. Division of Experimental Pathology, Department of Molecular and Experimental Medicine, The Scripps Research Institute, California 92037
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  • John J. Brems,

    1. The Scripps Clinic Center For Liver Diseases, Scripps Clinic and Research Foundation, La Jolla, California 92037
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  • Howard Takiff,

    1. The Scripps Clinic Center For Liver Diseases, Scripps Clinic and Research Foundation, La Jolla, California 92037
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  • Paul J. Pockros,

    1. The Scripps Clinic Center For Liver Diseases, Scripps Clinic and Research Foundation, La Jolla, California 92037
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  • Francis V. Chisari M. D.

    Corresponding author
    1. Division of Experimental Pathology, Department of Molecular and Experimental Medicine, The Scripps Research Institute, California 92037
    • Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10666 North Torrey Pines Road (SBR-10, Rm. SR106), La Jolla, CA 92037
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Abstract

The proliferative response of peripheral blood lymphocytes to the HBcAg was compared with serological, molecular and immunohistochemical parameters of hepatitis B virus infection and with biochemical and histological parameters of liver disease in a patient who received a completely human leukocyte antigen class I-mismatched liver allograft for fulminant hepatitis. The proliferative response increased progressively after transplantation, as hepatitis B virus infection became reestablished in the hepatic allograft. Strikingly, the HBcAg-specific T cells suddenly disappeared from the peripheral blood immediately before the acute onset of a severe necroinflammatory liver disease in which more than 80% of the hepatocytes expressed HBcAg. These observations are compatible with the hypothesis that human leukocyte antigen class I-independent hepatitis B virus-specific T cells might play a previously unsuspected role in the pathogenesis of hepatitis B virus-induced liver disease. (HEPATOLOGY 1993;18:491–496.)

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