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IgD‐receptor (IgD‐R) cross‐linking partially protects murine T cells from dexamethasone‐induced apoptosis
Author(s) -
Tamma Seetha M. Lakshmi,
Coico Richard F.
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1002492
Subject(s) - immunoglobulin d , biology , microbiology and biotechnology , apoptosis , antigen , fluorescein isothiocyanate , annexin , immune system , antibody , receptor , endocrinology , immunology , b cell , flow cytometry , biochemistry , fluorescence , physics , quantum mechanics
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.