MafB is a critical regulator of complement component C1q

Mai Thi Nhu Tran, Michito Hamada (), Hyojung Jeon, Risako Shiraishi, Keigo Asano, Motochika Hattori, Megumi Nakamura, Yuki Imamura, Yuki Tsunakawa, Risa Fujii, Toshiaki Usui, Kaushalya Kulathunga, Christina-Sylvia Andrea, Ryusuke Koshida, Risa Kamei, Yurina Matsunaga, Makoto Kobayashi, Hisashi Oishi, Takashi Kudo and Satoru Takahashi ()
Additional contact information
Mai Thi Nhu Tran: Faculty of Medicine, University of Tsukuba
Michito Hamada: Faculty of Medicine, University of Tsukuba
Hyojung Jeon: Faculty of Medicine, University of Tsukuba
Risako Shiraishi: Faculty of Medicine, University of Tsukuba
Keigo Asano: Faculty of Medicine, University of Tsukuba
Motochika Hattori: Faculty of Medicine, University of Tsukuba
Megumi Nakamura: Faculty of Medicine, University of Tsukuba
Yuki Imamura: Faculty of Medicine, University of Tsukuba
Yuki Tsunakawa: Faculty of Medicine, University of Tsukuba
Risa Fujii: Faculty of Medicine, University of Tsukuba
Toshiaki Usui: Faculty of Medicine, University of Tsukuba
Kaushalya Kulathunga: Faculty of Medicine, University of Tsukuba
Christina-Sylvia Andrea: Faculty of Medicine, University of Tsukuba
Ryusuke Koshida: Faculty of Medicine, University of Tsukuba
Risa Kamei: Faculty of Medicine, University of Tsukuba
Yurina Matsunaga: Faculty of Medicine, University of Tsukuba
Makoto Kobayashi: Faculty of Medicine, University of Tsukuba
Hisashi Oishi: Nagoya City University Graduate 24 School of Medical Sciences
Takashi Kudo: Faculty of Medicine, University of Tsukuba
Satoru Takahashi: Faculty of Medicine, University of Tsukuba

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: 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.

Date: 2017
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DOI: 10.1038/s41467-017-01711-0

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