ABSTRUCTPassive transfer of experimentally induced drug‐rash (GR) was studied in JY‐1 strain guinea pigs. Sulbenicillin (SBPC)‐induced GR was transferred into four of ten recipients by SBPC immunized cells. CET‐induced GR was transferred into twelve of seventeen recipients by CET‐immunized cells and accidentally transferred into two of fifteen recipients by CET‐immunized serum. However, CET‐induced GR was not successfully transferred by SBPC‐immunized cells, complete Freund's adjuvant (CFA)‐immunized cells, frozen and thawed materials, or sonicated cells of CET‐immunized cells. Anti‐CET antibody of CET‐immune serum was not detected by passive hemagglutination assay.CET‐immunized cells were separated into adherent and nonadherent fractions (Ad and Non‐Ad) in laboratory dishes coated with anti‐guinea pig γ‐globulin. CET‐induced GR was not transferred by Ad, but was transferred into eight of twenty‐two recipients by Non‐Ad. Only 4.6% of Non‐Ad cells were immunoglobulin bearing. Transferred GR appeared about 19–24 hr after GR‐elicitation. Erythema was paler than that of GR in actively sensitized guinea pigs.Microscopic examination of the skin taken about 24 hr after the cell transfer with systemic challenge revealed edema, dilation and compaction of capillaries, and diffuse lymphoid cell infiltration with a few eosinophils and basophils in the upper dermis. After about 48–72 hr, basophils were not confirmed as in actively sensitized animals. The count of peripheral leukocytes increased until 24 hr after GR elicitation in both recipients of immunized cells and immunized serum regardless of the severity of the GR reaction. It is likely that, in the transfer of drug‐induced GR, immune cells (probably primed T cells) which do not bear immunoglobulin have a significant role in GR, but serum factors a