The CD7- subset of CD4+ memory T cells is prone to accelerated apoptosis that is prevented by interleukin-15 (IL-15).

The CD7[sup -] subset of CD4[sup +] T cells reflects a stable differentiation state of post-thymic helper T cells with CD45R0[sup +]CD45RA[sup -] 'memory' phenotype. Here we report that CD4[sup +]CD7[sup -] T cells are prone to increased spontaneous apoptosis in vitro compared to CD4[sup +]CD7[sup +] T cells. Spontaneous apoptosis is prevented by IL-15, but not by IL-2. Moreover, IL-15 increases Bcl-2 and decreases CD95/Fas expression of CD7[sup -], but not of CD7[sup +] T cells. Because IL-15 is physiologically not secreted but expressed in a membranebound form, we cocultured T cells with TNF-α stimulated fibroblasts that expose membrane IL-15. TNF-α stimulated fibroblasts rescue CD4[sup +]CD7[sup -] Tcells from apoptosis whereas unstimulated fibroblasts do not. Rescue from apoptosis requires cell-cell contact and is abolished by addition of neutralizing antibodies to IL-15. We conclude that membrane IL-15 prevents accelerated apoptosis of CD4[sup +]CD7[sup -] T cells. This mechanism may contribute to accumulation of CD7[sup -] T cells in chronic inflammatory skin lesions. [ABSTRACT FROM AUTHOR]