Abstract
Immunization with allogeneic DBA/2 mastocytoma cells produced a decrease in thymic size and number of thymus cells and an increase in spleen size and number of spleen cells. The cells that remained in the thymus were more capable of inducing a graft-versus-host (GVH) reaction than thymus cells from untreated mice. Similar results were found if mice were treated with hydrocortisone. Hydrocortisone treatment before or after immunization with DBA/2 mastocytoma decreased the number and/or the activity of killer cells. Lymphocytes with killer cell activity against an allogeneic tumor were a different subpopulation of T cells than those that induced a GVH reaction. These results suggest that killer lymphocytes originate from precursor cells in the cortex of the thymus, are mobilized to the peripheral lymphoid tissues after immunization by mastocytoma cells, and are sensitive to hydrocortisone treatment. The mobilized lymphocytes are most likely incompletely differentiated cells of the killer lymphocyte class (T 1). Our results, however, did not prove that hydrocortisone sensitivity of these cells is related to their immaturity. Probably, there are at least two separate subpopulations of lymphocytes in the thymus: (a) T 2 cells (mature T), located in the medulla, that have vigorous capacity to induce GVH reaction, and (b) T 1 cells located in the cortex (incompletely differentiated), which need an additional maturation step to become mature T 2 cells: among these cells are those that become killer T-lymphocytes.
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