The mercy of adrenocortical tumor cells on lymphocytes

Immunologic escape includes the loss of Fas-receptor and the gain of Fas-li gand expression. Normal adrenal glands express the Fas-receptor and MHC cla ss II molecules in inner cortical zones. A distinctive feature of adrenocor tical tumors is the loss of MHC class II expression. Here we demonstrate loss of Fas and gain of Fas-ligand expression in the ad renocortical carcinoma cell line NCI-H295 by immunohistochemistry and RT-PC R. In a co-culture system of tumor cells and HLA-matched leukocytes, CD 8-p ositive or CD 4-positive lymphocytes, we examined the immunologic escape an d the ability to induce apoptosis in the immune cells. The direct co-cultur e with either leukocytes, CD 8-positive or CD 4-positive lymphocytes reduce d spontaneous apoptosis in immune cells from 49.9% to 13.0%, 8.6% and 15.3% , respectively, as determined by FAGS analysis of Annexin V binding and LDH release in the medium. In co-culture, cortisol secretion increased up to 2 00%. Cellular communication does not induce apoptosis in immune cells, but promo tes their survival. This may be due to partial HLA class I mismatches contr ibuting to immunologic activity. The viability of the tumor cells was not a ffected, and these cells were stimulated to secrete cortisol. In summary, i mmune escape of adrenocortical carcinomas may occur because of altered Fas/ Fas-L system expression and loss of MHC class H expression.