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Clin Immunol. 2018 Oct;195:1-7. doi: 10.1016/j.clim.2018.07.003. Epub 2018 Jul 4.

Hydroxychloroquine efficiently suppresses inflammatory responses of human class-switched memory B cells via Toll-like receptor 9 inhibition.

Author information

1
The First Department of Internal Medicine, School of Medicine, University of Occupational & Environmental Health, Japan, Kitakyushu 807-8555, Japan; Department of Endocrinology, Metabolism, Rheumatology and Nephrology, Faculty of Medicine, Oita University, Yufu 879-5593, Japan.
2
The First Department of Internal Medicine, School of Medicine, University of Occupational & Environmental Health, Japan, Kitakyushu 807-8555, Japan; Mitsubishi Tanabe Pharma, Yokohama 227-0033, Japan.
3
The First Department of Internal Medicine, School of Medicine, University of Occupational & Environmental Health, Japan, Kitakyushu 807-8555, Japan.
4
The First Department of Internal Medicine, School of Medicine, University of Occupational & Environmental Health, Japan, Kitakyushu 807-8555, Japan. Electronic address: tanaka@med.uoeh-u.ac.jp.

Abstract

Hydroxychloroquine is widely used for autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. Although B cells contribute to the pathogenesis of these diseases, the action of hydroxychloroquine on B cells remains unclear. Here we examined the effects of hydroxychloroquine on functions of B cell subsets. Hydroxychloroquine efficiently inhibited the mammalian target of rapamycin complex 1, differentiation of CD19+IgD-CD27+ class-switched memory B cells to plasmablasts and their IgG production, under stimulation with CpG, a Toll-like receptor (TLR)-9 ligand. Hydroxychloroquine also inhibited CpG-induced production of interleukin-6 and tumor necrosis factor-α in B cell subsets. Taken together, hydroxychloroquine markedly suppresses the TLR9-mediated human B cell functions during inflammatory processes. Based on our results, we believe that hydroxychloroquine can be beneficial in the treatment of B cell-mediated autoimmune diseases.

KEYWORDS:

Human B cell; Hydroxychloroquine; Plasmablast; Toll-like receptor 9

PMID:
29981383
DOI:
10.1016/j.clim.2018.07.003
[Indexed for MEDLINE]

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