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T Cells Marked by the 2H4 Antigen Function in Allosuppression

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Immunobiology of HLA

Abstract

A mouse monoclonal antibody (MAb), anti-2H4 (IgG1 subclass), has recently been described (1) that recognizes 200/220 kD glycoproteins (2) of the leukocyte common antigen/T200 family. The 2H4 antigen is found on 42% of unfractionated human T cells, 41% of CD4+ lymphocytes, 54% of CD8+ lymphocytes, and over 30% of both peripheral blood B cells and null cells. In a pokeweed mitogen system that measures B cell immunoglobulin production, the CD4+2H4+ cells were found to be inducers of suppression (1) and CD4+2H4− cells to be inducers of help (3). In the autologous mixed lymphocyte response (AMLR), CD8+2H4+ cells were found to have suppressor effector function (4). Additionally, in a concanavalin A− activated system, suppressor cell activity belonged to the 2H4+ subset of T cells (2). As the role of these subsets have not been established in alloimmunity, we studied the proliferative response and generation of suppressor cells in an allogeneic MLR using 2H4 enriched or depleted cells as the responding population.

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References

  1. Morimoto C, Letvin NL, Distaso JA, Aldrich WR, Schloss-man SF, The isolation and characterization of the human suppressor inducer T cell subset. J Immunol 1986; 134: 1508.

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  2. Morimoto C, Letvin NL, Rudd CE, Hagan M, Takeuchi T, Schlossman SF. The role of the 2H4 molecule in the generation of suppressor function in Con A-activated T cells. J Immunol 1986; 137: 3247.

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  4. Takeuchi T, Rudd CE, Schlossman SF, Morimoto C. Functional characterization of the 2H4 molecule in T8+ cells in the AMLR system (submitted).

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© 1989 Springer Science+Business Media New York

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Ramos, E.L., Turka, L.A., Leggat, J.E., Milford, E.L., Carpenter, C.B. (1989). T Cells Marked by the 2H4 Antigen Function in Allosuppression. In: Dupont, B. (eds) Immunobiology of HLA. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-39946-0_206

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  • DOI: https://doi.org/10.1007/978-3-662-39946-0_206

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-38980-5

  • Online ISBN: 978-3-662-39946-0

  • eBook Packages: Springer Book Archive

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