|
|
||||||||
Published online before print May 8, 2003
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

* Department of Microbiology and Immunology, CUNY Medical School, New York, New York; and
Department of Biomedical Sciences, C. W. Post, Long Island University, Brookville, New York
Correspondence: Richard F. Coico, Ph.D., Chairman, Department of Microbiology and Immunology, CUNY Medical School, 138 Street and Convent Avenue, New York, NY 10031. E-mail: coico{at}med.cuny.edu
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 annexinfluorescein 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, annexinFITC 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.
Key Words: IgD T cell activation Fas
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |