New Zealand Black (NZB) and NZB/NZB F1 hybrid mice (B/W) are genetically predisposed to a progressive disorder of immunologic regulation associated with a development of autoimmunity and lymphoid malignancy. We propose to define the defect associated with the observation of loss of suppression in NZB immunologic regulation. We will focus on the action of suppressive and enhancing factors released from cells following carrier priming. The interaction of these factors with splenic acceptor T cells will be our major focus. We hope that control of autoimmunity and malignant lymphoproliferation may be accomplished by the exogenous introduction of antigen specific suppressor factors into disease prone animals.