B Cell Depletion Inhibits Fibrosis via Suppression of Profibrotic Macrophage Differentiation in a Mouse Model of Systemic Sclerosis.


Journal

Arthritis & rheumatology (Hoboken, N.J.)
ISSN: 2326-5205
Titre abrégé: Arthritis Rheumatol
Pays: United States
ID NLM: 101623795

Informations de publication

Date de publication:
11 2021
Historique:
received: 09 05 2020
accepted: 25 04 2021
pubmed: 7 5 2021
medline: 16 12 2021
entrez: 6 5 2021
Statut: ppublish

Résumé

We undertook this study to investigate the effect of B cell depletion on fibrosis in systemic sclerosis (SSc) and its mechanism of action. Mice with bleomycin-induced SSc (BLM-SSc) were treated with anti-CD20 antibody, and skin and lung fibrosis were histopathologically evaluated. T cells and macrophages were cocultured with B cells, and the effect of B cells on their differentiation was assessed by flow cytometry. We also cocultured B cells and monocytes from SSc patients and analyzed the correlation between fibrosis and profibrotic macrophage induction by B cells. B cell depletion inhibited fibrosis in mice with BLM-SSc. B cells from mice with BLM-SSc increased proinflammatory cytokine-producing T cells in coculture. In mice with BLM-SSc, B cell depletion before BLM treatment (pre-depletion) inhibited fibrosis more strongly than B cell depletion after BLM treatment (post-depletion) (P < 0.01). However, the frequencies of proinflammatory T cells were lower in the post-depletion group than in the pre-depletion group. This discrepancy suggests that the effect of B cell depletion on fibrosis cannot be explained by its effect on T cell differentiation. On the other hand, profibrotic macrophages were markedly decreased in the pre-depletion group compared to the post-depletion group (P < 0.05). Furthermore, B cells from mice with BLM-SSc increased profibrotic macrophage differentiation in coculture (P < 0.05). In SSc patients, the extent of profibrotic macrophage induction by B cells correlated with the severity of fibrosis (P < 0.0005). These findings suggest that B cell depletion inhibits tissue fibrosis via suppression of profibrotic macrophage differentiation in mice with BLM-SSc, providing a new rationale for B cell depletion therapy in SSc.

Identifiants

pubmed: 33955200
doi: 10.1002/art.41798
doi:

Substances chimiques

Bleomycin 11056-06-7

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2086-2095

Informations de copyright

© 2021, American College of Rheumatology.

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Auteurs

Hiroko Numajiri (H)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Ai Kuzumi (A)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Takemichi Fukasawa (T)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Satoshi Ebata (S)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Asako Yoshizaki-Ogawa (A)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Yoshihide Asano (Y)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Yutaka Kazoe (Y)

Keio University School of Integrated Design Engineering, Tokyo, Japan.

Kazuma Mawatari (K)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Takehiko Kitamori (T)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Ayumi Yoshizaki (A)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

Shinichi Sato (S)

University of Tokyo Graduate School of Medicine, Tokyo, Japan.

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