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I-J: An Inducible Isomorphic Receptor Involved in the H-2-Restricted Cell Interaction and Inhibition

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H-2 Antigens

Part of the book series: NATO ASI Series ((NSSA,volume 144))

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Abstract

I-J still remains to be a premium grade paradox in H-2 genetics. Although it is not a direct product of H-2 genes, its polymorphism is clearly influenced by the intra H-2 genes. Recent functional data suggested that I-J is associated with the inducible T cells receptor for self class II antigens (1,2). It has been found that some of the anti-I-J monoclonal antibodies (mAb) could block the syngeneic and allogeneic mixed lymphocyte reactions (MLR) by reacting with the responder but not with stimulator cells (1). The I-J epitopes on responder cells were inducible in allogeneic bone marrow chimeras (2). Since some of the anti-I-J mAb were able to inhibit the H-2-restricted T helper cell (Th) function, we have recently tested their effect on Th and T cell clones derived from various intra H-2 recombinant mice and their bone marrow chimeras (3). The following are the summary of experimental results which suggest that I-J is an inducible isomorphic marker different from both class II products and conventional class II restricted T cell receptors.

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Reference

  1. W. Uracz, R. Abe, and T. Tada, Involvement of I-J epitopes in the self-and allo-recognition sites of T cells: blocking of syngenic and allogeneic mixed lymphocyte reaction-responder cells by monoclonal anti-I-J antibodies. Proc. Natl. Acad. Sci. USA 82:2905 (1985).

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© 1987 Springer Science+Business Media New York

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Tada, T., Asano, Y., Nakayama, T., Fujisawa, I. (1987). I-J: An Inducible Isomorphic Receptor Involved in the H-2-Restricted Cell Interaction and Inhibition. In: David, C.S. (eds) H-2 Antigens. NATO ASI Series, vol 144. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0764-9_43

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  • DOI: https://doi.org/10.1007/978-1-4757-0764-9_43

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-0766-3

  • Online ISBN: 978-1-4757-0764-9

  • eBook Packages: Springer Book Archive

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