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Nat Commun. 2017 Nov 22;8(1):1700. doi: 10.1038/s41467-017-01711-0.

MafB is a critical regulator of complement component C1q.

Author information

1
Department of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.
2
Department of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. hamamichi@md.tsukuba.ac.jp.
3
Laboratory Animal Resource Center, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. hamamichi@md.tsukuba.ac.jp.
4
Ph.D. Program in Human Biology, School of Integrative and Global Majors, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8577, Japan.
5
Department of Molecular and Developmental Biology, Faculty of Medicine, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.
6
Department of Comparative and Experimental Medicine, Nagoya City University Graduate 24 School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, 467-8601, Japan.
7
Laboratory Animal Resource Center, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.
8
Department of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. satoruta@md.tsukuba.ac.jp.
9
Laboratory Animal Resource Center, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. satoruta@md.tsukuba.ac.jp.
10
International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. satoruta@md.tsukuba.ac.jp.
11
Transborder Medical Research Center, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8577, Japan. satoruta@md.tsukuba.ac.jp.
12
Life Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, 1-1-1, Tennodai, Tsukuba, Ibaraki, 305-8577, Japan. satoruta@md.tsukuba.ac.jp.

Abstract

The transcription factor MafB is expressed by monocytes and macrophages. Efferocytosis (apoptotic cell uptake) by macrophages is important for inhibiting the development of autoimmune diseases, and is greatly reduced in Mafb-deficient macrophages. Here, we show the expression of the first protein in the classical complement pathway C1q is important for mediating efferocytosis and is reduced in Mafb-deficient macrophages. The efferocytosis defect in Mafb-deficient macrophages can be rescued by adding serum from wild-type mice, but not by adding serum from C1q-deficient mice. By hemolysis assay we also show that activation of the classical complement pathway is decreased in Mafb-deficient mice. In addition, MafB overexpression induces C1q-dependent gene expression and signals that induce C1q genes are less effective in the absence of MafB. We also show that Mafb-deficiency can increase glomerular autoimmunity, including anti-nuclear antibody deposition. These results show that MafB is an important regulator of C1q.

PMID:
29167450
PMCID:
PMC5700178
DOI:
10.1038/s41467-017-01711-0
[Indexed for MEDLINE]
Free PMC Article

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