Immune suppression gene on HLA-Bw54-DR4-DRw53 haplotype controls nonresponsiveness in humans to hepatitis B surface antigen via CD8+ suppressor T cells

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Abstract

The development of antiviral vaccines has been accelerated using monoclonal antibody and/or recombinant DNA techniques, the objective being to prevent grave viral infectious diseases, such as acquired immunodeficiency syndrome (AIDS), adult T-cell leukemia (ATL), and hepatitis B virus (HBV)—associated liver diseases. Certain proportions of individuals in the human population do not have any appreciable immune response to foreign antigens, either in cases of natural exposure or a planned immunization. Here we report that in the nonresponders to HB vaccine, there is an HLA-linked immune suppression gene for hepatitis B surface antigen (Is-HBsAg) controlling the nonresponsiveness to HBsAg through HBsAg-specific suppressor T cells. The Is-HBsAg is in strong linkage disequilibrium with the HLA-Bw54-DR4-DRw53 haplotype.

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    Moreover, the levels of antibody to HBsAg (anti-HBs) of an unknown further fraction of hepatitis B (HB) vaccinated persons fall considerably over time rendering them at potential risk of infection. The exact mechanisms underlying non responsiveness to HB vaccine are not known, however, certain human leukocyte antigen (HLA) and murine major histocompatibility complex haplotypes are related with HB vaccine non-responsiveness [4–7]. In addition, investigators have shown that immune responses to HBsAg are not properly induced in HB vaccine nonresponders due to inadequate priming of T and B lymphocytes [8,9].

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