title: Suppression of macrophage Ia antigen expression by endogenous interferon-alpha/beta.
abstract: Exogenous interferon-alpha (IFN-alpha) and interferon-beta (IFN-beta) (type I IFNs) are known to suppress the IFN-gamma-dependent expression of class II MHC (Ia) antigens on macrophages (M phi). We report here that the endogenous type I IFNs produced by M phi in response to IFN inducers regulate Ia expression of the M phi themselves. Coculture of M phi with IFN-gamma and polyinosinic-polycytidylic acid [poly(I):poly(C)] resulted in the reduction of Ia expression in comparison with those cultured without poly(I):poly(C). Pretreatment of M phi with poly(I):poly(C) or a bacterial lipopolysaccharide (LPS), which is also a potent IFN inducer, in vitro or in vivo, before being exposed to IFN-gamma was also effective in suppressing the Ia expression. Such suppression was abolished by the addition of anti-IFN-alpha/beta antibodies to the M phi culture along with IFN-gamma. M phi cultured with L-cell conditioned medium (LCM) containing M-CSF were less capable of expressing Ia antigens than those cultured without LCM. The Ia-expressing ability of LCM-treated M phi was also restored by the addition of anti-IFN-alpha/beta antibodies. M phi in the early stage of sterile inflammation were less responsive to IFN-gamma than those in the late stage. These results suggest that endogenous type I IFNs, which are produced in response to natural or synthetic IFN-inducers, regulate M phi Ia expression in an autocrinal manner.
authors.affiliation: Department of Zoology, Faculty of Science, Kyoto University.
authors.forename: T
authors.initials: T
authors.lastname: Kato
authors.forename: M
authors.initials: M
authors.lastname: Kitaura
authors.forename: K
authors.initials: K
authors.lastname: Inaba
authors.forename: Y
authors.initials: Y
authors.lastname: Watanabe
authors.forename: Y
authors.initials: Y
authors.lastname: Kawade
authors.forename: S
authors.initials: S
authors.lastname: Muramatsu
mesh_terms: D000210:Acute-Phase Reaction / Q000276:immunology; D000818:Animals; D002478:Cells, Cultured; D003470:Culture Media / Q000494:pharmacology; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis*; D007369:Interferon Inducers / Q000494:pharmacology; D007370:Interferon Type I / Q000096:biosynthesis / Q000502:physiology*; D007371:Interferon-gamma / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D011070:Poly I-C / Q000494:pharmacology
chemical_list: D003470:Culture Media; D000949:Histocompatibility Antigens Class II; D007369:Interferon Inducers; D007370:Interferon Type I; D008070:Lipopolysaccharides; D007371:Interferon-gamma; D011070:Poly I-C