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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Tran MTN,Hamada M,Jeon H,Shiraishi R,Asano K,Hattori M,Nakamura M,Imamura Y,Tsunakawa Y,Fujii R,Usui T,Kulathunga K,Andrea CS,Koshida R,Kamei R,Matsunaga Y,Kobayashi M,Oishi H,Kudo T,Takahashi Sdoi
10.1038/s41467-017-01711-0subject
Has Abstractpub_date
2017-11-22 00:00:00pages
1700issue
1issn
2041-1723pii
10.1038/s41467-017-01711-0journal_volume
8pub_type
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