The cellular infiltrate in the liver in auto-immune chronic active hepatitis: analysis with monoclonal antibodies

Authors

  • I. H. Frazer,

    1. Clinical Research Unit of the Walter and Eliza Hall Institute and the Royal Melbourne Hospital, and the Department of Nephrology, Royal Melbourne Hospital, Victoria, Australia
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  • I. R. Mackay,

    Corresponding author
    1. Clinical Research Unit of the Walter and Eliza Hall Institute and the Royal Melbourne Hospital, and the Department of Nephrology, Royal Melbourne Hospital, Victoria, Australia
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  • J. Bell,

    1. Clinical Research Unit of the Walter and Eliza Hall Institute and the Royal Melbourne Hospital, and the Department of Nephrology, Royal Melbourne Hospital, Victoria, Australia
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  • G. Becker

    1. Clinical Research Unit of the Walter and Eliza Hall Institute and the Royal Melbourne Hospital, and the Department of Nephrology, Royal Melbourne Hospital, Victoria, Australia
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Walter and Eliza Hall Institute of Medical Research Post Office, Royal Melbourne Hospital Victoria 3050 Australia

Abstract

ABSTRACT— The mononuclear cell infiltrate in the liver was analyzed, using a panel of monoclonal antibodies (MAbs) of known specificity, in 10 patients with auto-immune chronic active hepatitis and, for contrast, in 14 with other types of chronic parenchymal liver diseases. In all cases, the mononuclear cell (MNC) infiltrate in the liver consisted mostly of T lymphocytes. Helper (Th) cells were more frequent than suppressor/cytotoxic T cells (Tsc) in the portal tracts and cirrhotic scar tissue, while Tsc were more common in the hepatic parenchyma. The number of Tsc cells in the parenchyma was greatest in patients with histologically active CAH and least in patients with quiescent cirrhosis. “Plasmacytoid” cells with the morphology of plasma cells, a hallmark of the MNC infiltrate in auto-immune CAH, were more frequent in histologically active CAH than in quiescent cirrhosis. These plasmacytoid cells were T200 + ve, and hence of bone marrow origin, but the majority expressed neither membrane nor cytoplasmic immunoglobulin nor any lineage-specific marker antigens, and hence did not fulfil criteria for B lymphocytes; however, these cells were positive for OKT10 and HLA DR. No difference was evident between the MNC infiltrate in the liver in auto-immune CAH and that in the other acute or chronic liver diseases studied, including HBV-associated CAH; hence immunohistological studies do not point to any pathological processes uniquely responsible for the pattern of hepatocyte damage seen in auto-immune CAH.

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