The skin of CBA mice was painted with the contact sensitizing agent 4-ethoxymethylene-2-phenyloxazolone (oxazolone). One day later the regional lymph node cells were injected into the footpads of normal recipients. The recipients were tested 6 days later for contact sensitivity by challenging the ears with oxazolone and measuring the increase of ear thickness at 24 h. T cells and macrophages in the regional lymph nodes each independently gave rise to contact sensitivity in the recipient following injection into the footpad. This activity of T cells and macrophages was found in lymph nodes taken 1, 3 and 4 days after painting the donors. The role of T cells in the injected population was shown by purifying T cells by nylon-wool filtration and rosetting with sheep red cells coated with antibody and complement (EAC rosetting) and by destroyed T cells with anti-0 serum and complement. The activity of purified T cells resisted 2000 rad in vitro. The activity of cells from T-deprived (B) mice showed that a second cell type was important in the footpad transfer. This cell behaved like a macrophage, and not like a B cell, on EAC rosetting in the presence or absence of divalent cations and on treatment with silica and carrageenan--agents which damage macrophages. Our working hypothesis is that the footpad transfer may be caused independently by macrophages or T cells with oxazolone (probably linked to major histocompatibility complex antigens) on their surface and that these cells act by collaborating with T cells in the recipient which give rise to the effector cells for contact sensitivity.