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Abstract Number: 111

BAFF Inhibition Attenuates Fibrosis in Bleomycin-Induced Scleroderma Model Via Modulating the Regulatory and Effector B-Cell Balance

Takashi Matsushita1, Tadahiro Kobayashi2, Yasuhito Hamaguchi2, Minoru Hasegawa3, Manabu Fujimoto4 and Kazuhiko Takehara1, 1Kanazawa University, Department of Dermatology, Kanazawa, Japan, 2Department of Dermatology, Kanazawa University, Kanazawa, Japan, 3University of Fukui, Department of Dermatology, Fukui, Japan, 4University of Tsukuba, Faculty of Medicine, Department of Dermatology, Tsukuba, Japan

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: B cells, BAFF, IL-6 and systemic sclerosis

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Session Information

Date: Sunday, October 21, 2018

Session Title: Systemic Sclerosis and Related Disorders – Basic Science Poster I

Session Type: ACR Poster Session A

Session Time: 9:00AM-11:00AM

Background/Purpose: Systemic sclerosis (SSc) is an autoimmune disease characterized by skin and lung fibrosis. Over 90% of patients with SSc are positive for autoantibodies. In addition, serum B cell activating factor (BAFF) level is correlated with SSc severity and activity. Thus, B cells are considered to play a pathogenic role in SSc. However, there are two opposing subsets: regulatory B cells (Bregs) and effector B cells (Beffs). IL-10-producing Bregs negatively regulate the immune response, while IL-6-producing Beffs positively regulate. Therefore, a protocol that selectively depletes Beffs would represent a potent therapy for SSc. The aim of this study was to investigate the roles of Bregs and Beffs in SSc, and to provide a scientific basis for developing a new treatment strategy targeting B cells.

Methods: The bleomycin-induced scleroderma model was induced in the mice with a B cell-specific deficiency in IL-6 or IL-10. We also examined whether BAFF regulates cytokine-producing B cells and its effects on scleroderma model.

Results: Serum IL-6 levels gradually increased with the development of fibrosis in bleomycin-induced scleroderma mice, while serum IL-10 levels did not. IL-6-producing Beffs increased in Spleen and the inflamed skin of scleroderma model. The skin and lung fibrosis was attenuated in B cell-specific IL-6-deficient mice, whereas B cell-specific IL-10-deficient mice showed more severe fibrosis. BAFF stimulation increased Beffs and decreased Bregs. By contrast, BAFF antagonist (BAFFR-Fc) increased Bregs and decreased Beffs (Fig 1). Furthermore, BAFF antagonist attenuated skin and lung fibrosis in scleroderma model via modulating the regulatory and effector B-cell balance (Fig 2).

Conclusion: The current study indicates that Beffs play a pathogenic role in scleroderma model while Bregs play a protective role (Fig 3). BAFF inhibition is a potential therapeutic strategy for SSc via alteration of B cell balance.


Disclosure: T. Matsushita, None; T. Kobayashi, None; Y. Hamaguchi, None; M. Hasegawa, None; M. Fujimoto, None; K. Takehara, None.

To cite this abstract in AMA style:

Matsushita T, Kobayashi T, Hamaguchi Y, Hasegawa M, Fujimoto M, Takehara K. BAFF Inhibition Attenuates Fibrosis in Bleomycin-Induced Scleroderma Model Via Modulating the Regulatory and Effector B-Cell Balance [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/baff-inhibition-attenuates-fibrosis-in-bleomycin-induced-scleroderma-model-via-modulating-the-regulatory-and-effector-b-cell-balance/. Accessed December 14, 2019.
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