We have previously shown that T cells from mice immunized with a high molecular weight polysaccharide (PS) isolated from Pseudomonas aeruginosa can inhibit bacterial growth in vitro and adoptively protect non-immune mice in vivo. The current proposal seeks to analyze how T cells are activated by PS and to clone and analyze the activity of regulatory T cells that control this response. We propose a model of T cell activation by PS that involves cross-linking of Fc receptors (FcR) on T cells that have been "pre-armed" with P. aeruginosa-specific antibody produced in undetectable amounts in the spleen. Cross-linking of the FcR results in secretion of an antibacterial lymphokine. This model is supported by several findings: 1. T cell immunity is demonstrable only when there is evidence of B cell activation, although in some cases, this evidence is indirect since specific antibody cannot be detected. 2. PS does not bind to gene products of the major histocompatibility complex. Activation of T cells cannot occur via the T cell receptor. 3. Removal of, or enrichment for, immune T cells bearing FcR removes or enriches antibacterial T cell activity, respectively. The planned studies will (a) evaluate the effect of immunization of FcR expression by T cells, (b) examine the ability of FcR for different immunoglobulin classes to generate antibacterial activity, (c) attempt to elicit T cell antibacterial activity by cross-linking FcR without bacterial products, and (d) seek to directly demonstrate the presence of P. aeruginosa-specific antibody on the surface of T cells. The effect of cloned suppressor and contrasuppressor T cell lines on FcR expression will also be studied.