Journal Article

MafB is a critical regulator of complement component C1q

Tsunakawa Yuki, 小林 麻己人, Hamada Michito, Shiraishi Risako, Kudo Takashi, 濱田 理人, Tran Mai Thi Nhu, Hattori Motochika, 越田 隆介, Koshida Ryusuke, 工藤 崇, Imamura Yuki, Usui Toshiaki, Kobayashi Makoto, Kulathunga Kaushalya, Kamei Risa, Andrea Christina-Sylvia, Fujii Risa, Matsunaga Yurina, Asano Keigo, Oishi Hisashi, Takahashi Satoru, Nakamura Megumi, Jeon Hyojung, 高橋 智

2017

Overview

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.

• Publisher: Nature,Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
• Subject: 631/250/249/1313 / 631/250/2504/342 / 631/45/612/113 / Apoptosis / Autoimmune diseases / Complement / Complement activation / Complement component C1q / Gene expression / Humanities and Social Sciences / Macrophages / Mice / Monocytes / multidisciplinary / Rodents / Science / Science (multidisciplinary)