Regulatory role of IgE-binding factors from rat T lymphocytes. I. Mechanism of enhancement of IgE response by IgE-potentiating factor.
T lymphocytes in the mesenteric lymph nodes of rats infected with Nippostrongylus brasiliensis spontaneously released a soluble factor that selectively potentiated the IgE-forming cell response of antigen-primed cells to homologous antigen. The factor could enhance the IgE response of DNP-OA-primed cells to DNP-HSA and T cell-replacing factor. In contrast, the treatment of OA-primed T cells with the factor failed to enhance either the IgE or IgG response of the mixture of DNP-KLH primed cells and OA-primed T cells to DNP-OA. The results collectively suggested that the target cells of the IgE-potentiating factor are B cells. Indeed, IgE potentiating factor was absorbed by B cells rather than T cells or thymocytes. Evidence was obtained that IgE-potentiating factor could be absorbed by IgE-bearing B cells or IgE-coupled Sepharose, indicating that the factor had affinity for IgE. It appeared that the potentiating factor bound to IgE-bearing B cells and selectively enhanced the differentiation of IgE-B cells to IgE-forming cells. It was also found that the major source of the factor was Fc epsilon R-bearing T cells.
D000042:Absorption; D000818:Animals; D000921:Antibody-Producing Cells / Q000276:immunology; D001402:B-Lymphocytes / Q000166:cytology; D001666:Binding Sites, Antibody; D002454:Cell Differentiation; D002474:Cell-Free System; D004136:Dinitrobenzenes / Q000276:immunology; D006725:Hookworm Infections / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis; D010047:Ovalbumin / Q000276:immunology; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology*
D004136:Dinitrobenzenes; D007073:Immunoglobulin E; D010047:Ovalbumin