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Analysis of the (H‐2b× H‐2k)F1Restricted Response to Insulin

The aim of these studies was to characterize the (H‐2b× H‐2k)F1‐unique restriction element(s) responsible for presentation of bovine insulin (BI) to a long‐term cultured T‐cell line (BK‐BI‐1.2). (B10.BR × bm12)F1 spleen cells, which express a normal Abα Akβ molecule but a mutated Akα AAbm12β product on their cell surface, were perfectly able to act as BI‐presenting cells. Antibody inhibition experiments with antibodies directed at I‐Ak products revealed that monoclonal antibody 10–2.16, which reacts with the Akβ polypeptide chain, abrogated BI‐directed T‐cell proliferation, whereas antibody H116–32.R5 with specificity for the Akα chain was not inhibitory. These results identified the AbαAkβ complex as restriction structure. Recognition of BI in the context of the Abα Akβ molecule depended on the glutamic acid residue in position 4 of the A chain of bovine insulin. Twenty to twenty‐five percent of the secondary proliferative response of (B10 × B10.BR)F1 lymph node T cells primed with BI in vivo was directed at the A4 determinant, suggesting that BK‐BI‐1.2 T blasts are representative of T‐cell clones with measurable frequency. In (B10.BR × bm12)F1 mice, which lack a functional Abα Abβ restriction element, up to 80% of the proliferative response was dependent on the A4 epitope.