Contact and delayed hypersensitivity in the mouse. 3. Depression of contact sensitivity by pre-treatment with antigen and the restoration of immune competence in tolerant mice by normal lymphoid and bone marrow cells.

Contact sensitivity was produced in mice by applying an alcoholic solution of picryl chloride or 2-phenyl-4-ethoxymethylene oxazolone (oxazolone) to the abdominal wall. It was assessed by painting the ear with the contact sensitizing agent dissolved in olive oil and measuring the increase in ear thickness 24 hours later. Contact sensitivity to picryl chloride was depressed by pre-treatment with the sulphonic acid derivative of picric acid. Complete depression was obtained when either two large doses or multiple small doses were given and in the former case this complete depression was still present 6 weeks after the last injection of the sulphonic acid. Similar pre-treatment with oxazolone depressed contact sensitivity to oxazolone in some but not all mice. Pre-treatment with the folic acid antagonist amethopterin before and during sensitization almost completely abolished contact sensitivity, while a single larger dose given 48 hours before sensitization only had a small effect. Mice whose immune response to picryl chloride had been depressed by pretreatment with sulphonic acid and methotrexate were used to study restoration of immune competence by normal lymphoid cells. No restoration was observed when unirradiated recipients were used. However, a mixture of lymph node and bone marrow cells and, to a lesser extent thymus and bone marrow cells, restored immune competence to picryl chloride in irradiated recipients. It was concluded that irradiation favoured the restoration of immune competence by normal lymphoid cells and that a mixture of lymph node and possibly thymus cells with bone marrow cells was able to cause restoration.