Donor skin grafts from B10.D2 (H-2d) mice were placed on (C57BL/6J X A/J)F, (B6AF1) (H-2a, b) recipients; B10.BR (H-2k) skin grafts were placed on B6AF1 recipients as specificity controls. A single pool of high titered B6AF1 anti-B10.D2 allo-antiserum was used for enhancement. The H-2K.31 specificity on 51Cr-labeled P815 tumor cells was used as a target to assay daily for T cell cytotoxicity in draining lymph node and spleen cells of grafted mice. Peak 51Cr release developed by 11 days in local lymph nodes and by 13 days in spleens of nonenhanced mice. In enhanced mice, peak cytotoxic responses were delayed until 17 days in local lymph nodes and until 18 days in the spleen. To create an efferent block of ongoing cellular immune responses, alloantisera was administered after skin grafting. To assess cellular immunity, a constant 4-mg B10.D2 tumor implant was used. Antiserum administered with tumor challenge allowed progressive tumor growth when tumor and antiserum were given early after skin grafting, but tumors were rejected if tumor and antiserum were given 10 or 15 days after grafting. Also, antiserum prolonged skin graft survival in mice passively transferred with normal splenocytes but did not abrogate the shortened graft survival time seen if mice were given cytotoxic splenocytes. Enhancing antibody was effective during the sensitization phase of skin graft rejection but did not block in vivo during the effector phase of T cell cytotoxicity.