The dissection of antigen-driven immunologic responses placed into the intricate multicompartmentalized framework of the in vivo environment presents a dimension of complexity that is not generally appreciated. This associates with the ability of lymphoid cells to recirculate and home and is best exemplified with cell-mediated immune responses where the imposition of a physical barrier between "immune" cells and the stimulating antigen will totally abrogate a functional protective immune state. Therefore, the presence of accessory cells, the appropriate cellular interactions and collaborations, and the selection and differentiation of clonally-derived precursors for effector cells is insufficient for functional in vivo cell-mediated immune responses. The acquired or inherently induced capacity of lymphocytes to selectively extravasate into nonlymphoid sites of antigen deposition represents an essential component for effective in vivo immune function. To advance our understanding of syngeneic host-tumor interactions requires a full appreciation of selective lymphoid cell movement. This knowledge must be integrated into the already appreciated cellular interactions and responses that are taking place. Together, a more complete picture of the immunologic apparatus can be obtained and manipulated. The investigation of ultraviolet radiation (UVR) carcinogenesis has already provided us with an appreciation for the delicate interrelationship taking place among the host, the tumor, and the carcinogen (UVR). We have recently determined that one process mediated by this physical agent results in an induced alteration in lymphocyte recirculation pathways. This finding has direct immunologic implications. A detailed analysis of this phenomenon and its importance in antitumor immune responses represents the major objective of this research. These studies will be complemented with experiments designed to address a number of basic questions associated with the nature and regulation of lymphocyte homing pathways. (SR)