β-Endorphin stimulates Ia expression on mouse B cells by inducing interleukin-4 secretion by CD4+ T cells

article
In the present study we show that the opioid peptide β-endorphin (β-End) enhances Ia expression on murine B cells in cultures of unseparated spleen cells, mediated by low concentrations of IL4 in the absence of antigenic or mitogenic stimulation. Since this effect was not found with purified B cells and no enhancement of IL-4 receptor expression on B cells could be observed, we studied the effect of β-End on IL-4 production. To this end, purified CD4+ T cells were stimulated with suboptimal concentrations of Con A in the presence of irradiated spleen cells. It was indeed shown that β-End enhances IL-4 production. To establish the role of macrophages in this process, we measured IL-1 and IL-6 production under the influence of β-End. Splenic adherent cells as well as peritoneal macrophages produced higher levels of IL-1 and IL-6 in response to β-End, whereas IL-1 was shown to enhance Ia expression similar to β-End. Using anti-IL-6 it was demonstrated that IL-6 was required for the stimulation of Ia expression by β-End. It is concluded that a local increase in β-End may result in upregulation of Ia expression on B cells, thereby most likely improving their antigen-presenting capacity. Chemicals/CAS: beta endorphin, 59887-17-1; concanavalin A, 11028-71-0; naloxone, 357-08-4, 465-65-6; beta-Endorphin, 60617-12-1; Histocompatibility Antigens Class II; interleukin 1 receptor antagonist protein; Interleukin-1; Interleukin-4, 207137-56-2; Interleukin-6; Naloxone, 465-65-6; Sialoglycoproteins
TNO Identifier
232103
ISSN
00088749
Source
Cellular Immunology, 149(1), pp. 180-192.
Pages
180-192
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