Letter | Published:

Inhibition by sera and soluble antigens of T-cell-mediated cytotoxicity against leukaemia-associated antigens

Naturevolume 266pages727729 (1977) | Download Citation



INTEREST in the regulation of T-cell-mediated cytotoxicity by the major histocompatibility complex (MHC) genes stems from the discovery of (1) an H–2 restriction of T-cell-mediated cytotoxicity, that is sensitising cells, effector cells and target cells need to be syngeneic at the H–2 locus, especially at the D and or K regions of the MHC1–5 for effective killing and (2) inhibition of T-cell-mediated cytotoxic reactions against syngeneic tumours with alloantibodies to H–2 antigens specific for the tumour cells6,7. Different origins have been proposed for the tumour-associated antigens (TAA), and the most favourable model is a modified H–2 antigen or an adaptor–antigen complex4–7. This issue has important implications for tumour immunology, and so we have evaluated the validity of the inhibition of cytotoxicity by serum at the effector phase level; investigated afferent interference by serum of the cell-mediated cytotoxic response, and studied the inhibition of cell-mediated cytotoxic reactions with soluble antigens. We report here that there is a lack of H–2 restriction of T-cell-mediated cytotoxicity to TAA, and that TAA seems to differ from H–2 antigens. This implies that T-cell recognition is not entirely regulated by the MHC genes.

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  1. Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, 20014



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