Balb/c or A/He mice immunized with the phosphorylcholine (PC) binding IgA myeloma protein (T15), produced by the TEPC-15 myeloma, produce antibody which specifically neutralizes mouse antibody to PC and suppresses the antibody response of normal mice or their spleen cells in culture to immunization with PC. Conceptually this antibody to T15 functions as an antibody directed against the receptor for PC and is referred to as ARA. ARA given passively to adult mice causes reversible short term suppression which lasts about as long as the passively given antibody persists. In contrast, ARA given to neonatal mice causes suppression of many months duration, apparently by depletion of the clone of cells reactive to PC. Suppression produced in neonates is prevented by normal adult mouse serum or normal mouse IgG suggesting that the mechanism of clonal depletion may be by antibody dependent cell mediated cytotoxicity. Individual mice immunized repeatedly with PC produce antibody to PC and later ARA. The appearance of serum ARA correlates with a declining response to PC suggesting that autogenous ARA may regulate the response to PC. Our aims now are to assess the role of ARA in the regulation of the antibody response in immunized, tolerant and paralyzed mice; to characterize the cell types required for the ARS response, to characterize the target specificity of ARA, and finally, to extrapolate our findings to other systems. We have devised a means of enumerating cells producing ARA and we must now develop procedures for quantitating ARA in the presence of specific antibody and possibly antigen.