Specificity of antigen binding by T cells; competition between soluble and Ia‐associated antigen

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Abstract
Competitive antigen binding experiments were performed with purified T and B cells of C3H.SW (H‐2b) mice. As antigen, (T, G)‐A–L [poly‐L(Tyr, Glu)‐poly‐DL‐Ala–poly‐L Lys] was used, both in an Ia‐containing form, released by adherent cells (IAC, Puri and Lonai, Eur. J. Immunol. 1980.10: 273), and in regular solution. It was found that regular (T, G)‐A–L did not compete with the binding of 125I‐labeled‐IAC‐(T, G)‐A–L even at a 104‐fold excess, whereas IAC‐(T, G)‐A–L inhibited binding at 10‐fold excess. The specificity of (T, G)‐A–L binding to high‐responder T and B cells was compared by using related branched synthetic copolymers as competitors. B cells cross‐reacted with (T, G)‐A–L, (H, G)‐A–L, (Phe, G)‐A–L, (G)‐A–L and (T, G)‐Pro–L. In contrast, antigen‐binding C3H.SW T cells cross‐reacted only with (T, G)‐A–L and (Phe, G)‐A–L, to both of which they are Ir gene‐controlled high responders. Evidence for the Ir gene control of IAC‐binding T cells was obtained by showing that high × low‐responder F1 hybrid T cells preferentially bind IAC‐(T, G)‐A–L processed by processor cells deriving from the high‐responder parental strain. These data are interpreted to suggest that T cells have high affinity for antigen plus self Ia complexes, whereas they have a much lower, if any, affinity for free antigen. It also follows from the results that the structure of the complex ligand may have a role in defining the specificity, H‐2 restriction and Ir gene control of T cells.