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Beta-endorphin stimulates Ia expression on mouse B cells by inducing interleukin-4 secretion by CD4+ T cells.

Abstract：

:In the present study we show that the opioid peptide beta-endorphin (beta-End) enhances Ia expression on murine B cells in cultures of unseparated spleen cells, mediated by low concentrations of IL-4 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 beta-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 beta-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 beta-End. Splenic adherent cells as well as peritoneal macrophages produced higher levels of IL-1 and IL-6 in response to beta-End, whereas IL-1 was shown to enhance Ia expression similar to beta-End. Using anti-IL-6 it was demonstrated that IL-6 was required for the stimulation of Ia expression by beta-End. It is concluded that a local increase in beta-End may result in upregulation of Ia expression on B cells, thereby most likely improving their antigen-presenting capacity.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

van den Bergh P,Rozing J,Nagelkerken L

doi

10.1006/cimm.1993.1146

subject

Has Abstract

pub_date

1993-06-01 00:00:00

pages

180-92

issue

1

eissn

0008-8749

issn

1090-2163

pii

S0008874983711469

journal_volume

149

pub_type

杂志文章

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