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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Dysregulated heme oxygenase-1low M2-like macrophages augment lupus nephritis via Bach1 induced by type I interferons

Fig. 5

Schema describing our hypothesis of BTB and CNC homology 1 (Bach1)-mediated M2 dysregulation in lupus nephritis. Type I interferons are highly produced by plasmacytoid dendritic cells in systemic lupus erythematosus [1]. The secreted interferons suppress heme oxygenase (HO)-1 expression in CD163+ M2-like macrophages via induction of HO-1 transcriptional repressor Bach1. These aberrantly functional HO-1 low M2-like macrophages produce inflammatory cytokines such as interleukin (IL)-6, which is facilitated by reduced HO-1 expression. Bach1 also has the property of modulating M2-like macrophage differentiation, as suggested in our Bach1−/− mouse experiments

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