In the mouse, allergic contact dermatitis to the strong contact allergen dinitrofluorobenzene is maximal 5 to 6 days after sensitization and rapidly fades in the succeeding days. It has been proposed that this loss of T-cell reactivity depends on feedback inhibition by anti-idiotypic antibody of the expression of allergic contact dermatitis. We have examined this question by studying the course of allergic contact dermatitis in mice made B-cell deficient by the chronic administration from birth of a heterologous antibody with specificity for mouse IgM. We found in these mice a spontaneous loss of allergic contact dermatitis comparable to that seen in normal intact mice. This implies that the rapid rise and fall of contact sensitivity in the mouse is not necessarily mediated by B cells (or B-cell products) and is compatible with its control, at least in part, by T-suppressor cells.

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