Delayed hypersensitivity has been characterized primarily by responses “in vivo” in either man or experimental animals. Typically, therefore, the slowness of the indurated response to intradermal injection of antigen, the mononuclear nature of the cellular infiltrate, the lack of correlation between the extent of induration and the amount of antibody, and the passive transfer of hypersensitivity with lymphoid cells and not with antiserum all constitute delayed hypersensitivity “in vivo”. Animals possessing these characteristics may also possess an “in vitro” correlate, namely, the inhibition of migration of lymphoid cells in the presence of specific antigen. Initially, cell migration from fragments of lymphoid organs was inhibited in tissue culture by specific antigen (1–3). This inhibition of migration could not be induced by circulating antibody, and apparently therefore is not associated with conventional circulating globulins (4). Additional “in vitro” systems for the study of migration inhibition in delayed hypersensitivity have recently been introduced (5, 6).