Abstract
The recombinase-activating genes, RAG-1 and RAG-2, can be expressed by a subset of B cells within germinal centers, where they mediate secondary V(D)J rearrangements. This receptor revision mechanism could serve either receptor diversification or tolerance-induced functions. Alternatively, it might rescue those cells the receptors of which have been damaged by somatic mutation. Less is known about the occurrence of similar mechanisms in T cells. Here we show that mature T cells with defective TCR surface expression can express RAG genes and are capable of initiating secondary V(D)J rearrangements. The possibility that a cell rescue mechanism based on the generation of a novel Ag receptor might be active in peripheral T cells is envisaged.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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CD3 Complex / biosynthesis*
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CD4 Antigens / biosynthesis*
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Cell Differentiation / immunology
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DNA-Binding Proteins / biosynthesis
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DNA-Binding Proteins / genetics*
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Enzyme Activation / genetics
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Enzyme Activation / immunology
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Gene Expression Regulation, Enzymologic / immunology
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Gene Rearrangement, T-Lymphocyte*
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Homeodomain Proteins / biosynthesis
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Homeodomain Proteins / genetics*
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Humans
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Nuclear Proteins
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Receptors, Antigen, T-Cell, alpha-beta / biosynthesis
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Receptors, Antigen, T-Cell, alpha-beta / genetics*
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T-Lymphocyte Subsets / cytology
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T-Lymphocyte Subsets / enzymology*
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T-Lymphocyte Subsets / immunology*
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T-Lymphocyte Subsets / metabolism
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Transposases / genetics
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Transposases / metabolism*
Substances
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CD3 Complex
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CD4 Antigens
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DNA-Binding Proteins
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Homeodomain Proteins
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Nuclear Proteins
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RAG2 protein, human
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Receptors, Antigen, T-Cell, alpha-beta
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V(D)J recombination activating protein 2
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RAG-1 protein
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Transposases