| Title: | Low disease activity of microscopic polyangiitis in patients with anti-myosin light chain 6 antibody that disrupts actin rearrangement necessary for neutrophil extracellular trap formation |
| Authors: | Yoshinari, Miku Browse this author |
| Nishibata, Yuka Browse this author |
| Masuda, Sakiko Browse this author →KAKEN DB |
| Nakazawa, Daigo Browse this author →KAKEN DB |
| Tomaru, Utano Browse this author →KAKEN DB |
| Arimura, Yoshihiro Browse this author →KAKEN DB |
| Amano, Koichi Browse this author →KAKEN DB |
| Yuzawa, Yukio Browse this author →KAKEN DB |
| Sada, Ken-Ei Browse this author →KAKEN DB |
| Atsumi, Tatsuya Browse this author →KAKEN DB |
| Dobashi, Hiroaki Browse this author →KAKEN DB |
| Hasegawa, Hitoshi Browse this author →KAKEN DB |
| Harigai, Masayoshi Browse this author →KAKEN DB |
| Matsuo, Seiichi Browse this author |
| Makino, Hirofumi Browse this author →KAKEN DB |
| Ishizu, Akihiro Browse this author →KAKEN DB |
| Keywords: | MPA |
| NETs |
| ANETA |
| Anti-MYL6 antibody |
| Issue Date: | 16-Dec-2022 |
| Publisher: | BioMed Central |
| Journal Title: | Arthritis Research & Therapy |
| Volume: | 24 |
| Issue: | 1 |
| Start Page: | 274 |
| Publisher DOI: | 10.1186/s13075-022-02974-9 |
| PMID: | 36527167 |
| Abstract: | Background: Neutrophil extracellular traps (NETs) are critically involved in microscopic polyangiitis (MPA) pathogenesis, and some patients with MPA possess anti-NET antibody (ANETA). Anti-myosin light chain 6 (MYL6) antibody is an ANETA that affects NETs. This study aimed to determine the significance of anti-MYL6 antibody in MPA. Methods: The influence of anti-MYL6 antibody on NET formation and actin rearrangement necessary for NET formation was assessed by fluorescent staining. An enzyme-linked immunosorbent assay was established to detect serum anti-MYL6 antibody, and the prevalence of this antibody in MPA was determined. Furthermore, the disease activity and response to remission-induction therapy of MPA were compared between anti-MYL6 antibody-positive and anti-MYL6 antibody-negative MPA patients. Results: Anti-MYL6 antibody disrupted G-actin polymerization into F-actin, suppressing phorbol 12-myristate 13-acetate-induced NET formation. Serum anti-MYL6 antibody was detected in 7 of 59 patients with MPA. The Birmingham vasculitis activity score (BVAS) of anti-MYL6 antibody-positive MPA patients was significantly lower than anti-MYL6 antibody-negative MPA patients. Among the nine BVAS evaluation items, the cutaneous, cardiovascular, and nervous system scores of anti-MYL6 antibody-positive MPA patients were significantly lower than anti-MYL6 antibody-negative MPA patients, although other items, including the renal and chest scores, were equivalent between the two groups. The proportion of patients with remission 6 months after initiation of remission-induction therapy in anti-MYL6 antibody-positive MPA patients was significantly higher than in anti-MYL6 antibody-negative MPA patients. Conclusions: Collective findings suggested that anti-MYL6 antibody disrupted actin rearrangement necessary for NET formation and could reduce the disease activity of MPA. |
| Type: | article |
| URI: | http://hdl.handle.net/2115/87589 |
| Appears in Collections: | 保健科学院・保健科学研究院 (Graduate School of Health Sciences / Faculty of Health Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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