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on High Affinity Fc Receptor Expression in Healthy Controls and Multiple Sclerosis Patients1
*
Unité 365, Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie, Section de Recherche,
Laboratoire d’Immunologie Cellulaire, Fédération de Neurologie et INSERM CJF 9608, Hôpital Pitié-Salpêtrière, and
Unité d’Immuno-Allergie, Institut Pasteur, Paris, France
Monocyte-macrophage activation by IFN-
is characterized by a
pronounced increase of high affinity Fc receptors for IgG (FcRI),
capable of triggering respiratory burst, phagocytosis, Ab-dependent
cytotoxicity, and release of proinflammatory cytokines. In view of the
antagonism of IFN-ß on IFN- action, of interest in the chronic
inflammatory disorder multiple sclerosis, we examined the possible
effect of IFN-ß on IFN- induction of FcRI gene expression. We
found that IFN-ß significantly down-regulated IFN--induced FcRI
surface expression in peripheral blood monocytes from healthy donors,
in a dose- and time-dependent manner. This down-regulation of FcRI
surface levels did not correspond to a decrease in FcRI mRNA,
suggesting a posttranscriptional effect of IFN-ß. Down-regulation of
FcRI surface expression correlated with diminished cellular
signaling through FcRI, since the IFN--induced increase in Fc
receptor-triggered respiratory burst was nearly completely abrogated by
simultaneous addition of IFN-ß. Finally, the same antagonism between
both IFNs on FcRI surface expression was observed in peripheral
blood monocytes derived from multiple sclerosis patients; inhibition by
IFN-ß was even increased (82 ± 11%), as compared with healthy
controls (67 ± 4%). These results may partially help explain the
beneficial effect of IFN-ß in multiple
sclerosis.
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