The cellular basis of the mechanism of action of cortisone acetate on contact sensitivity to oxazolone in the mouse.
The cellular aspects of the action of cortisone acetate on the induction and recall phases of contact sensitivity to oxazolone in the mouse have been investigated. The present findings indicate that cortisone has a much less damaging effect on the thymus-derived than on the non-thymus-derived lymphoid population in the peripheral lymphoid organs. It is also shown that the permanent immunosuppressive effect of cortisone given before sensitization is associated with the virtual absence of polymorph infiltration of the dermis, absence of epidermal vesication at the site of application of oxazolone and a considerable reduction in the amount of lymphocyte transformation amongst the thymus-derived cells in the draining lymph node. The temporary immunosuppression observed when cortisone is given just before recall is also associated with absence of polymorph infiltration of the dermis and of epidermal vesication at the test site. It is suggested that in the present model of cell-mediated immunity cortisone is immunosuppressive mainly by preventing the antigenic stimulus from being received. Some of the mechanisms by which cortisone could achieve this form of immunosuppression are discussed.