Abstract

AbstractContact sensitivity in the mouse is assessed by the increase of ear thickness 24 hours after challenge with antigen and can be passively transferred by T cells in the lymph nodes and spleen of immunized mice. The lymph node cells of mice pretreated with picrylsulfonic acid specifically depress the passive transfer of contact sensitivity to picryl chloride by immune cells.“Suppressor” lymph node cells from mice injected with picrylsulfonic acid (−6 days) and painted with picryl chloride (‐1 day) were incubated in vitro for 48 hours. Immune lymph node cells incubated in these supernatants have reduced ability to transfer contact sensitivity. This suppression is specific and passive transfer of contact sensitivity to 4‐ethoxymethylene‐2‐phenyloxazolone is unaffected by incubation of immune cells in supernatant. Control supernatants from the cells of mice which did not receive picrylsulfonic acid or were not painted shortly before harvesting were inactive.The suppressor activity is absorbed by peritoneal exudate cells and these then acquire the ability to suppress passive transfer‐“arming for suppression”. Normal and immune lymph node cells, and spleen cells do not become inhibitory under similar conditions.The suppressor activity of suppressor supernatants (which contain 10 % fetal calf serum) withstands freeze drying, heating at 56 °C and trypsin. Its production is T dependent and is abolished by treatment with anti‐Θ serum and complement. The hypothesis is put forward that the active factor in suppressor supernatants is a specific T cell product either free or combined with antigen.

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