IgD-receptor (IgD-R) cross-linking partially protects murine T cells from dexamethasone-induced apoptosis

Based on our previous findings that immunoglobulin D (IgD) receptor (IgD-R) cross-linking with oligomeric IgD (IgD-R-xL) led to T cell activation, we examined the effect of IgD-R-xL on the expression of Fas antigen and apoptosis induction. In splenic T cells, IgD-R-xL followed by dexamethasone (dex) treatment resulted in a decreased percentage of Fas-positive cells as well as a decreased mean fluorescence intensity (P<0.05) when compared with cells treated with dex alone. There are significant differences in annexin-fluorescein isothiocyanate (FITC) and phosphatidylinositol (PI) staining between samples treated with dex alone and IgD-R-xL followed by dex-treated samples (P<0.05), suggesting a protective role for IgD-R-xL. No significant differences are seen in Fas antigen expression, annexin-FITC staining, and/or PI staining in murine T hybridoma (7C5) cells cultured under similar conditions (P<0.07). We hypothesize that ligation of IgD-R may predispose antigen-specific T lymphocytes for survival during primary immune responses when IgD-positive B cells serve as antigen-presenting cells.