Administration of an appropriate dose of anti-lymphocyte serum (ALS) results in a selective enhancement of the primary, secondary, and adoptive secondary IgE anti-2,4-dinitrophenyl (DNP) antibody responses of mice to DNP-key-hole limpet hemocyanin (KLH); in contrast, responses of the IgG class were not similarly affected under the conditions employed. The enhancing activity of ALS could be completely absorbed with mouse thymocytes, but not with erythrocytes, plasma cells, or brain cells; in fact, preabsorption with brain cells consistently increased the enhancing activity of ALS.

Although the initial interpretation of such findings was the ALS enhanced IgE antibody production by preferential elimination of suppressor cells, further analysis revealed that such an interpretation is inadequate to explain the phenomenon. Thus, lymphoid cells from otherwise unprimed donors that had been pretreated with various forms of ALS were found to be consistently capable of exerting some type of enhancing activity on the IgE responses of syngeneic DNP-KLH-primed spleen cells when the two populations were adoptively transferred concomitantly into irradiated recipients. Such observations indicate that ALS may facilitate antibody production not only by possible elimination of suppressor T cell activity, as heretofore concluded, but also by induction of lymphoid cells capable of actively potentiating the IgE response. Such ALS-induced “potentiator” cells were not readily susceptible to depletion by anti-ϑ serum plus complement treatment and do not appear to act directly on DNP-specific IgE B lymphocytes in the primed cell population.

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