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Cooperation between thymic-derived cells (T cells) and bone marrow-derived precursors of antibody-forming cells (B cells) is not thought to be required for an antibody response to Type III pneumococcal polysaccharide, or SSS-III 1 (1-3). Yet treatment with antilymphocyte or antithymocyte serum (ALS or ATS), which causes a depletion of T cells (4-10), produces a significant increase in the magnitude of both the plaque-forming cell (PFC) and the serum antibody response to this antigen (11)(12)(13)(14) and an increase in the serum antibody response to keyhole limpet hemocyanin (15) and polyvinylpyrolidone (16). With respect to the PFC response to SSS-III, such enhancement can be abrogated by the infusion of syngeneic thymocytes; however, the infusion of peripheral white blood cells, a population reported to contain 60-90% T cells (17,18), results in additional enhancement (12).On the basis of these findings, we hypothesized that two functionally distinct types of cells (suppressor and amplifier cells2), presumably both thymic-derived, act in an opposing manner to regulate the magnitude of the antibody response to SSS-III by B cells; the enhancement produced after treatment with either ALS or ATS is apparently due to the inactivation of cells that normally exert a negative, rather than a positive, influence on the magnitude of the antibody response elicited after immunization (12).