The induction of primary responses has been reviewed elsewhere (Sprent and Webb, 1987). In brief, primary responses of T and B cells are initiated when antigen localizes in discrete microenvironments of the lymphoid tissues, especially the periarteriolar lymphocyte sheaths of the spleen and the paracortex of the lymph node (LN). These areas are perfused by naive recirculating lymphocytes, and recognition of antigen in these sites causes selective sequestration of antigen-reactive T and B cells. Trapping of B cells is presumed to reflect contact with free antigen, whereas T cell trapping is induced by major histocompatibility complex-bound antigenic peptides displayed by interdigitating dendritic cells. Trapping of T and B cells is followed by rapid proliferation of both cell types, B (cell proliferation being controlled by help from antigenspecific T cells. Under the influence of lymphokines, both cell types undergo marked expansion, the extent of expansion being a reflection of antigen concentration and the affinity of the responding cells. The proliferating cells acquire various effector functions and are released into the circulation and the central lymphatic vessels after a period of several days. Effector cells express various homing/adhesion molecules that are lacking on naive cells, and tht? se newly synthesized homing molecules enable effector cells to penetrate the walls of capillary blood vessels