biostudies-literatureKishimoto DYokohama Foundation for Advanced Medical ScienceNaito FoundationJapanese Society for the Promotion of Science Grants-in-Aid for Scientific ResearchTakeda Medical Research FoundationJapan Agency for Medical Research and DevelopmentJapan Intractable Diseases Research FoundationJapan Rheumatic Disease FoundationUehara Memorial FoundationMochida Memorial Foundation for Medical and Pharmaceutical ResearchJapan Society for the Promotion of Science64https://www.ebi.ac.uk/biostudies/studies/S-EPMC5894134biostudies-literatureUnknown20(1)BACKGROUND:Innate immunity including macrophages (Mϕ) in lupus nephritis (LN) has been gaining attention, but roles of Mϕ in LN remain uncertain. METHODS:Immunohistochemical staining was performed to determine CD68, CD163, heme oxygenase (HO)-1 (a stress-inducible heme-degrading enzyme with anti-inflammatory property), pSTAT1, and CMAF-expressing Mϕ in the glomeruli of patients with LN. Effects of type I interferons on the expression levels of CD163, HO-1, BTB and CNC homology 1 (Bach1; a transcriptional HO-1 repressor), interleukin (IL)-6, and IL-10 by human M2-like Mϕ, which were differentiated in vitro from peripheral monocytes with macrophage colony-stimulating factor, were assessed by RT-PCR and immunocytostaining. Clinical manifestations, anti-double-stranded DNA (anti-dsDNA), and loArthritis research & therapyDysregulated heme oxygenase-1low M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons.PMC58941342686075616K086987790011965264614692646146826713136Nagahama KYoshimi RNakajima HKunishita YKirino YNakano HAoki ITakeno MTakase-Minegishi KKishimoto DIgarashi KKato ITamura MfalseDysregulated heme oxygenase-1low M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons.BACKGROUND:Innate immunity including macrophages (Mϕ) in lupus nephritis (LN) has been gaining attention, but roles of Mϕ in LN remain uncertain. METHODS:Immunohistochemical staining was performed to determine CD68, CD163, heme oxygenase (HO)-1 (a stress-inducible heme-degrading enzyme with anti-inflammatory property), pSTAT1, and CMAF-expressing Mϕ in the glomeruli of patients with LN. Effects of type I interferons on the expression levels of CD163, HO-1, BTB and CNC homology 1 (Bach1; a transcriptional HO-1 repressor), interleukin (IL)-6, and IL-10 by human M2-like Mϕ, which were differentiated in vitro from peripheral monocytes with macrophage colony-stimulating factor, were assessed by RT-PCR and immunocytostaining. Clinical manifestations, anti-double-stranded DNA (anti-dsDNA), and lo2018-01-01T00:00:00Z2018 Apr2025-04-26T06:58:46.54Z2019-03-26T23:29:29ZS-EPMC58941342963609110.1186/s13075-018-1568-1