PRESENCE OF AN ANTIGEN-SPECIFIC T-CELL SUBSET THAT FORMS IGE-SUPPRESSIVE FACTOR AND IGG-SUPPRESSIVE FACTOR ON ANTIGENIC-STIMULATION

  • 1 January 1985
    • journal article
    • research article
    • Vol. 135  (2) , 922-929
Abstract
B6D2F1 mice were given 3 i.v. injections of ovalbumin [OA], an antigen-specific T cell clones were established from their spleen cells. One of the FcR+ (Fc receptor) T cell clones formed IgE-binding factors on incubation with OA-pulsed syngeneic macrophages. Neither soluble antigen nor macrophages alone induced factor formation. T cell hybridomas were constructed by fusion of the antigen-specific T cell clone with BW 5147 cells. Among 11 T cell hybridomas established, 6 clones produced IgE-binding factors on incubation with OA-pulsed BDF1 macrophages. Mouse IgE also induced the same hybridoma to form IgE-binding factors. The majority of IgE-binding factors formed by 2 T hybridomas and by those produced by the parent T cell clone had affinity for peanut agglutinin, but for neither lentil lectin nor concanavalin A. These hybridomas and the original T cell clone spontaneously released glycosylation-inhibiting factor, which inhibits the assembly of N-linked oligosaccharide(s) on IgE-binding factors. On antigenic stimulation, the T cell hybridomas produced both IgE-binding factors and IgG-binding factors. The IgE-binding factors consisted of 3 species with MW of 60,000, 30,000 and 15,000. Both the 60K (kilodalton) and 15K IgE-binding factors selectively suppressed the IgE response of DNP(dinitrophenyl)-OA-primed rat mesenteric lymph node cells, whereas IgG-binding factors selectively suppressed the IgG response. The results indicate that antigen-primed FcR+ T cells produced IgE-suppressive factors and IgG-suppressive factors on antigenic stimulation. The T cell hybridomas were not committed to suppressive activity. When the hybridomas were stimulated by antigen in the presence of glycosylation-enhancing factor [GEF], the 60K, 30K and 15K IgE-binding factors formed by the cells selectively potentiated the IgE response. IgG-binding factors formed by the cells in the presence of GEF failed to suppress the IgG response. It appears that antigen-specific FcR+ T cells regulate the antibody response through the formation of Ig-binding factors, but that the function of the cells could be switched from suppression to enhancement, depending on the environment of the cells.

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