The effector phase of an antigen specific immune response, involving multiple interactions between cells, is described as being either humoral or cell mediated. The pathological consequences of an immune response are mainly determined by the effector pathway chosen. Although the effector mechanisms are well characterized, the mechanism by which a response to a given antigen or infectious agent is directed into the humoral or cell mediated mode is not known. The major focus of this proposal is to study the mechanism by which the immune system directs a particular responses into one of these 2 pathways. Both types of effector responses depend upon the activation of CD4+ T cells. CD4+ T cells are helper cells for B cells, mediators of delayed type hypersensitivity responses, and helper cells for cytolytic T cell responses. Analysis of cloned T cells have shown that not all cloned lines mediate all these functions. Cloned CD4+ T cells can be divided into 2 subsets which are functionally distinct. One subset induces antigen specific B cells to secrete and the other subset mediates delayed type hypersensitivity responses, suppresses antibody production and kills appropriate target cells. These two subsets appear to induce effector responses which are primarily humoral or cell mediated. In this proposal, the activation requirements of the 2 functionally distinct subset will be studied in an attempt to understand the control of humoral and cell mediated responses.