Immunoglobulin-specific T-B cell interaction III. B cell activation by immunoglobulinrecognizing T cell clones

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Abstract
Immunoglobulin (Ig)-specific T-B cell interactions were studied in the model of T cell recognition of Ig ϰ chain Igϰ-1b allotype in Igϰ-1-congenic rats. Using Igϰ-1b-recognizing major histocompatibility complex (MHC)-restricted T helper clones from August rats we have shown that Igϰ-1b+ B cells from congenic August. 1b rats presented Igϰ-1b epitope of the processed self-synthesized Ig to T clones. This interaction was found to be a bidirectional regulatory event inducing specific MHC-dependent proliferation of both interacting T cell and B cell as well as Ig(Igϰ-1b) synthesis. Small Igϰ-1b+ B cells were capable of inducing T clone proliferation and becoming activated in response to the same T clone. Limiting dilution analysis suggested that every tenth cell in Igϰ-1b+ B cell population is involved in this interaction. The bystander activation of Igϰ-1a+ B cells by T clones in the presence of irradiated Igϰ-1b+ spleen cells, if observed, was less than the level of specific Igϰ-1b+ B cell proliferation. In contrast to a 20-fold increase of Ig(Igϰ-1b) levels upon stimulation of Igϰ-1b+/1a+ B cell population from heterozygous (August × August.1b)F1 rats by T clones, a “nonspecific” increase of Ig(Igϰ-1a) was not observed. This result demonstrates the requirement for direct T-B contact for B cell activation to occur. The data suggest a great functional potency of T-B interactions mediated by T cell recognition of Ig-derived peptide/MHC class II complexes on the B cell surface. The implication of the data for idiotypic regulation enables us to propose the existence of putative idiopeptidic network T-B cell interactions.