A Novel Mechanism of Somatic Rearrangement Predicted by a Human T-Cell Antigen Receptor β-Chain Complementary DNA
- 7 June 1985
- journal article
- research article
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 228 (4704) , 1204-1206
- https://doi.org/10.1126/science.3839095
Abstract
The T-cell antigen receptor is a cell surface molecule vital in mediating the cellular immune response. The arrangement and rearrangement of the gene segments encoding the beta-chain polypeptide of the receptor are similar to those of immunoglobulin gene segments. The two constant region genes of the human T-cell antigen receptor are 8 kilobases apart with a cluster of joining segments located 5' of each constant region gene. Although most beta-chain gene rearrangements involve the variable, diversity, and joining segments, analysis of a beta-chain complementary DNA clone suggests the occasional occurrence of another type of rearrangement.Keywords
This publication has 18 references indexed in Scilit:
- Homologous Recombination Catalyzed by Mammalian Cell Extracts in VitroScience, 1984
- Identification of a diversity segment of human T-cell receptor β-chain, and comparison with the analogous murine elementNature, 1984
- Localization of a T-cell receptor diversity-region elementNature, 1984
- Genomic organization and sequence of T-cell receptor β-chain constant- and joining-region genesNature, 1984
- Mouse T cell antigen receptor: Structure and organization of constant and joining gene segments encoding the β polypeptideCell, 1984
- Somatic recombination in a murine T-cell receptor geneNature, 1984
- Sequence relationships between putative T-cell receptor polypeptides and immunoglobulinsNature, 1984
- Isolation of cDNA clones encoding T cell-specific membrane-associated proteinsNature, 1984
- The mouse T cell receptor: Comparison of MHC-restricted receptors on two T cell hybridomasCell, 1983
- The human T cell receptor: Appearance in ontogeny and biochemical relationship of α and β subunits on IL-2 dependent clones and T cell tumorsCell, 1983