Abstract
The 70-kilodalton heat shock proteins may be expressed on the cell surface by an unknown mechanism and may interact with CD3+4-8- T cell receptor-alpha beta-killer (DNT) cells. In this interaction, certain cellular nascent or mutant peptides may be important (the complexes of 70-kilodalton heat shock protein and cellular peptides directly interact with DNT cells). The results imply that the interaction between 70 kilodalton heat shock proteins and DNT cells may also work in graft rejection. By using antibodies that react with the cell surface-expressed 70-kilodalton heat shock proteins, one may overcome graft rejection.
MeSH terms
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Animals
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Antibodies, Monoclonal / immunology
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Antibodies, Monoclonal / toxicity
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CD4-CD8 Ratio / drug effects
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Flow Cytometry
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Gene Expression Regulation / genetics
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Gene Expression Regulation / immunology
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Graft Rejection / immunology
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Heat-Shock Proteins / immunology
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Heat-Shock Proteins / metabolism*
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Killer Cells, Natural / drug effects
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Killer Cells, Natural / immunology*
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Membrane Proteins / immunology
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Membrane Proteins / metabolism*
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Mice
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Mice, Nude
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Molecular Chaperones
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Molecular Weight
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Rats
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Rats, Wistar
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Receptor-CD3 Complex, Antigen, T-Cell / drug effects
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Receptor-CD3 Complex, Antigen, T-Cell / immunology*
Substances
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Antibodies, Monoclonal
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Heat-Shock Proteins
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Membrane Proteins
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Molecular Chaperones
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Receptor-CD3 Complex, Antigen, T-Cell