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

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.