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Expression of Delta Opioid Receptors and Transcripts by Splenic T Cells
Author(s) -
SHARP BURT M.,
LI MING D.,
MATTA SHAN G.,
McALLEN KATHY,
SHAHABI NAHID A.
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb05441.x
Subject(s) - ionomycin , δ opioid receptor , t cell , receptor , t cell receptor , cd3 , microbiology and biotechnology , biology , cell growth , immune system , immunology , opioid , biochemistry , cd8 , intracellular
A bstract : Delta opioid receptors (DORs) and preproenkephalin‐A‐derived opiate peptides are expressed by mononuclear cells in various lymphoid organs. DOR ligands modulate a variety of immune functions, such as T‐cell proliferation, calcium mobilization, and cytokine production. recently, quiescent T‐cells were found to express low levels of DOR transcripts, which increased due to the following: cell culture of unstimulated murine splenocytes (depending on cell density); cross‐linking the T‐cell receptor (TCR) with anti‐CD 3 ‐ε and a single in vivo exposure to staphylococcal enterotoxin B (SEB). Enhanced expression of DOR mRNA was mediated transcriptionally. Moreover, PMA + ionomycin, which mimic the proliferative signal of anti‐CD 3 , inhibited the expression of DOR mRNA. Using semiquantitative immunofluorescence to detect DORs, SEB was found to increase the fraction of T cells that expressed DOR and to enhance the relative level of DOR expression per T cell. Previous studies have shown that DOR agonists inhibited the anti‐CD 3 ‐stimulated production of interleukin‐2 and T‐cell proliferation. Therefore, the enhanced expression of DORs by activated T cells may be capable of downregulating the T‐cell activation program.