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  • Title: Role of the 2H4 molecule in the activation of suppressor inducer function.
    Author: Morimoto C, Matsuyama T, Rudd CE, Forsgren A, Letvin NL, Schlossman SF.
    Journal: Eur J Immunol; 1988 May; 18(5):731-7. PubMed ID: 2967762.
    Abstract:
    The monoclonal antibody anti-2H4 recognizes a 220-kDa and 200-kDa glycoprotein and subdivides T4+ cells into distinct subpopulations: the T4+2H4+ inducer of suppression and the T4+2H4- inducer of help. The T4+2H4+ subset has been shown to play a crucial role in the activation of T8+ suppressor cells. In the present study, we attempted to determine whether the 2H4 molecule itself may be involved in initial triggering of suppressor inducer function. The results show that the addition of anti-2H4 antibody to a mixture of B and T cells resulted in a marked suppression of pokeweed mitogen-driven Ig synthesis. When anti-2H4 was added to B cell cultures containing T4+2H4+ or T4+2H4- cells but lacking T8 cells, no suppression was generated. In addition to the requirement for T8 cells, no suppression was generated if T4+2H4+ cells were absent. These results suggest that the anti-2H4 antibody contributes to the activation of the T4+2H4+ lymphocyte subset, which in turn induces T8 cells to suppress B cell Ig synthesis. Biochemical analysis of the T4+2H4+ subset of lymphocytes indicated that the in vitro addition of anti-2H4 antibody resulted in an increased expression of the 220-kDa and 200-kDa structure on T4 cells. We conclude that perturbation of the 2H4 molecule may potentiate the activation of the suppressor inducer subset and that the T200 molecule may be directly involved in suppressor inducer function.
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