Article
Antagonistic action of IFN-beta and IFN-gamma on high affinity Fc gamma receptor expression in healthy controls and multiple sclerosis patients
Registro en:
Antagonistic action of IFN-beta and IFN-gamma on high affinity Fc gamma receptor expression in healthy controls and multiple sclerosis patients. Journal of Immunology, v. 161, n. 3, p. 1568-1574, 1998.
0022-1767
Autor
Van Weyenbergh, Johan Jozef Rosa Maria
Lipinski, Pawel
Abadie, Annie
Chabas, Dorothé
Blank, Ulrich
Liblau, Roland
Wietzerbin, Juana
Resumen
Monocyte-macrophage activation by IFN-g is characterized by a pronounced increase of high affinity Fc receptors for IgG
(FcgRI), capable of triggering respiratory burst, phagocytosis, Ab-dependent cytotoxicity, and release of proinflammatory cytokines.
In view of the antagonism of IFN-b on IFN-g action, of interest in the chronic inflammatory disorder multiple sclerosis, we
examined the possible effect of IFN-b on IFN-g induction of FcgRI gene expression. We found that IFN-b significantly downregulated
IFN-g-induced FcgRI surface expression in peripheral blood monocytes from healthy donors, in a dose- and timedependent
manner. This down-regulation of FcgRI surface levels did not correspond to a decrease in FcgRI mRNA, suggesting
a posttranscriptional effect of IFN-b. Down-regulation of FcgRI surface expression correlated with diminished cellular signaling
through FcgRI, since the IFN-g-induced increase in Fcg receptor-triggered respiratory burst was nearly completely abrogated by
simultaneous addition of IFN-b. Finally, the same antagonism between both IFNs on FcgRI surface expression was observed in
peripheral blood monocytes derived from multiple sclerosis patients; inhibition by IFN-b was even increased (82 6 11%), as
compared with healthy controls (67 6 4%). These results may partially help explain the beneficial effect of IFN-b in multiple
sclerosis.