Inducer and Suppressor T-Cells in Hepatitis B Virus-induced Liver Disease

Authors

  • Howard C. Thomas,

    Corresponding author
    1. Departments of Medicine and Immunology, Royal Free Hospital, Hampstead, London NW3 2QG, England and the Immunobiology Division, Orthopharmaceutical Corporation, Raritan, New Jersey 08869
    • Howard C. Thomas, Academic Department of Medicine, The Royal Free Hospital, Pond Street, Hampstead, London NW3 20G England.
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    • Howard C. Thomas is a Senior Wellcome Fellow.

  • David Brown,

    1. Departments of Medicine and Immunology, Royal Free Hospital, Hampstead, London NW3 2QG, England and the Immunobiology Division, Orthopharmaceutical Corporation, Raritan, New Jersey 08869
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  • Guitaine Routhier,

    1. Departments of Medicine and Immunology, Royal Free Hospital, Hampstead, London NW3 2QG, England and the Immunobiology Division, Orthopharmaceutical Corporation, Raritan, New Jersey 08869
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  • George Janossy,

    1. Departments of Medicine and Immunology, Royal Free Hospital, Hampstead, London NW3 2QG, England and the Immunobiology Division, Orthopharmaceutical Corporation, Raritan, New Jersey 08869
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  • Patrick C. Kung,

    1. Departments of Medicine and Immunology, Royal Free Hospital, Hampstead, London NW3 2QG, England and the Immunobiology Division, Orthopharmaceutical Corporation, Raritan, New Jersey 08869
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  • Gideon Goldstein,

    1. Departments of Medicine and Immunology, Royal Free Hospital, Hampstead, London NW3 2QG, England and the Immunobiology Division, Orthopharmaceutical Corporation, Raritan, New Jersey 08869
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  • Sheila Sherlock

    1. Departments of Medicine and Immunology, Royal Free Hospital, Hampstead, London NW3 2QG, England and the Immunobiology Division, Orthopharmaceutical Corporation, Raritan, New Jersey 08869
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Abstract

During acute type B hepatitis, the proportion of inducer to cytotoxic/suppressor T-cells is decreased due to an increase in the concentration of suppressor cells. Similar changes are seen in chronically infected subjects with evidence of active viral replication (HBeAg positive) and chronic hepatitis of varying severity. This imbalance of the regulatory cells returns to normal when viral replication decreases during the recovery phase of acute hepatitis and in patients who become chronic carriers with minimal liver disease (HBeAb positive patients). Patients in whom viral replication has subsided (HBeAb positive) but who continue to exhibit chronic active liver disease have increased inducer to cytotoxic/suppressor cell ratios due to a decrease in the concentration of the cytotoxic/suppressor cell population. Further studies are needed to determine whether these alterations of the regulatory cells of the immune system are a causal factor influencing the duration of active hepatitis B virus replication and the degree of inflammatory liver damage, or merely changes secondary to the presence of a replicating virus.

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