Abstract
The organization of the mouse T cell receptor (TCR) genes has been extensively reviewed (Hood 1985). The structure of the TCR alpha (α), beta (β) and gamma (γ) genes is analogous to the immunoglobulin (Ig) gene organization in the mouse. This homology probably reflects similar requirements for diversity in binding antigen. The major source of diversity for Ig genes comes from (1) multiple germline variable (VK, Vλ and VH) regions, diversity (DH) regions and joining (Jj(, JX and Jh) elements; (2) combinatorial joining of V, D and J; (3) somatic mutation and (4) multiple alleles present in inbred and wild mice (Tonegawa 1983). Preliminary findings among the TCRα and β chains of the mouse inbred strains indicate fewer germline variable (VTα, VTβ) genes are available (30–40 each) (Becker 1985; Barth 1985; Behlke 1985a) than VK and VH genes (100–300 each) (Valbuena 1978; Cory 1981; Brodeur and Riblet 1984). Furthermore, studies indicate that the frequency of somatic mutation in TCRα and TCRβ chain genes although present is as much as 10% or less than that of Ig genes (Augustin and Sim 1984; Ikuta 1985).
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Huppi, K., D’Hoostelaere, L.A., Jouvin-Marche, E. (1986). The Context of T Cell Receptor β Chain Genes Among Wild and Inbred Mouse Species. In: Potter, M., Nadeau, J.H., Cancro, M.P. (eds) The Wild Mouse in Immunology. Current Topics in Microbiology and Immunology, vol 127. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71304-0_34
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DOI: https://doi.org/10.1007/978-3-642-71304-0_34
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