Abrogation and reconstitution of nonresponsiveness: a correlation with high network connectivity

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Abstract
A monoclonal antibody (Fd‐B2) to ferredoxin, which bears an idiotype scarcely expressed in any of a wide variety of mouse strains, is able to markedly enhance the response to ferredoxin of both high‐responder and intermediate‐responder strains. A rabbit anti‐idiotype serum to Fd‐B2 also specifically enhances the response to ferredoxin in such mice. Most remarkably, the treatment of nonresponder T cells by either the idiotype (Fd‐B2) plus complement or anti‐idiotype antiserum plus complement causes them to be responsive in adoptive transfer experiments. The two responding populations (idiotype‐treated and anti‐idiotype‐treated) can then be combined to reconstitute the nonresponsive state. When the nonresponders are treated with either Fd‐B2 idiotype plus complement or anti‐idiotype plus complement and subsequently respond, the idiotype of the anti‐ferredoxin antibody produced does not bear the Fd‐B2 idiotype. We interpret the results as being consistent with a model in which the unresponsive state for ferredoxin is a state of high network connectivity of the fer‐redoxin‐specific T cells.

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