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Expression of Delta Opioid Receptors by Splenocytes from SEB-Treated Mice and Effects on Phosphorylation of MAP Kinase

2000; Elsevier BV; Volume: 205; Issue: 2 Linguagem: Inglês

10.1006/cimm.2000.1717

1090-2163

Nahid Shahabi, Kathy McAllen, Shannon G. Matta, Burt M. Sharp,

Pharmacological Receptor Mechanisms and Effects

Delta opioid receptors (DORs) are known to modulate multiple T-cell responses. However, little is known about the expression of these receptors. These studies evaluated the expression of DOR mRNA and protein after a single in vivo exposure to staphylococcal enterotoxin B (SEB). SEB (20 μg, ip) significantly enhanced splenocyte DOR mRNA expression 8 and 24 h after injection. SEB also increased the fractions of the total splenocyte (5 to 20%) and T-cell (8 to 50%) populations expressing DOR protein. In saline-treated animals, DOR relative fluorescence intensity per cell was 11.1 ± 0.62 units (mean ± SEM), increasing to 16.1 ± 1.7 after exposure to SEB. DOR fluorescence intensity significantly increased to 33.5 ± 2.0 units in a subpopulation of T-cells. Thus, SEB significantly increased DOR expression in vivo, affecting both mRNA and protein levels primarily within the T-cell population. To determine whether T-cell DORs modulate the activity of extracellular-regulated kinases (ERKs), the phosphorylation of ERKs 1 and 2 was studied using splenocytes from SEB-treated mice. At concentrations from 10−8 to 10−6 M, [d-Ala2-d-Leu5]-enkephalin, a selective DOR agonist, significantly inhibited anti-CD3-ϵ-induced phosphorylation of the ERKs. Therefore, the DORs expressed by activated T-cells are capable of attenuating T-cell activation that depends on ERK phosphorylation.