Critical role of lectin pathway mediated by MBL-associated serine proteases in complement activation for the pathogenesis in systemic lupus erythematosus
Yuko Asanuma,
Kazuhisa Nozawa,
Masakazu Matsushita,
Makio Kusaoi,
Yoshiyuki Abe,
Ken Yamaji,
Naoto Tamura
Affiliations
Yuko Asanuma
Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan; Corresponding author. Department of Internal Medicine and Rheumatology, Juntendo University, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Kazuhisa Nozawa
Department of Internal Medicine and Rheumatology, Juntendo University Koshigaya Hospital, Saitama, Japan
Masakazu Matsushita
Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan
Makio Kusaoi
Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan
Yoshiyuki Abe
Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan
Ken Yamaji
Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan
Naoto Tamura
Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan
In complement activation system, although the classical pathway has shown to play a critical role for the pathogenesis of SLE, the role of lectin pathway has remained unknown in the pathogenesis of SLE. As Mannose-binding lectin-associated serine proteases (MASPs) are associated with activation of the lectin pathway, we conducted this study to clarify MASPs associations in the pathogenesis of SLE. We evaluated the serum level of MASPs (MASP-1 and MASP-2) in total 68 SLE patients consisting of 15 patients with biopsy-confirmed membranous lupus nephritis (M-LN), 35 patients with biopsy-confirmed proliferative lupus nephritis (P-LN), and 18 SLE patients without LN (non-LN). Our data showed that the serum levels of MASPs were reduced in both P-LN and non-LN although those of M-LN were not reduced. Our data show that the lectin pathway mediated by MASPs plays a critical role for the pathogenesis of SLE except for M-LN.
