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Abstract Number: 1082

Type I/II Interferon Commits to Abnormal Expression of Chemokine Receptor on B Cells in Patients with Systemic Lupus Erythematosus

Maiko Yoshikawa1, Shingo Nakayamada2, Satoshi Kubo3, Shigeru Iwata4, Kei Sakata5, Yusuke Miyazaki3, Kazuhisa Nakano2, Kazuyoshi Saito6 and Yoshiya Tanaka7, 1The First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, Kitakyusyu, Japan, 2First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan, 3The First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan, 4First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan, 5Mitsubishi Tanabe Pharma Corporation, Tokyo, Japan, 6University of Occupational and Environmental Health, Japan, Kitakyushu, Japan, 7University of Occupational and Environmental Health, Kitakyushu, Japan

Meeting: 2016 ACR/ARHP Annual Meeting

Date of first publication: September 28, 2016

Keywords: B cells, Chemokine Receptors, SLE and interferons

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Session Information

Date: Monday, November 14, 2016

Session Title: B Cell Biology and Targets in Autoimmune Disease - Poster I: SLE and Sjögren's

Session Type: ACR Poster Session B

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

Background/Purpose:  Systemic lupus erythematosus (SLE) is characterized by an expanded population of peripheral memory B cells. However, little is known about the qualitative abnormality of B cells associated with the pathogenesis of SLE. We assessed the subset of B cells by expression of chemokine receptors in patients with SLE and performed in vitro analysis to assess the differentiation mechanisms of those subsets.

Methods: PBMCs obtained from subjects with 56 patients with SLE, 31 patients with rheumatoid arthritis (RA) and 20 healthy donors (HD) were analyzed. Circulating B cell subsets were categorized by expression of chemokine receptors such as CXCR3 and CXCR5. Additionally, pan B cells obtained from HDs were cultured 4 days under stimulation with B cell receptor, co-stimulatory molecules and cytokines such as IL-21 and type I/II interferons (IFNs), and we assessed the expression of chemokine receptors such as CXCR3 and CXCR5 and transcription factors such as T-bet and Bcl-6 by multi-color flow cytometry.

Results: 1) The proportion of effector memory B cells (EM B cells; CD19+CD20+IgD–CD27–) has significantly increased in SLE compared to HD and RA (p<0.01). 2) The proportion of CD19+CD20+CXCR5–CXCR3– B cells and CD19+CD20+ CXCR5–CXCR3+ B cells has significantly increased in SLE, compared to HD and RA, which were remarkably noted in CD19+CD20+IgD–CD27+/- memory B cells (p<0.01). 3) CXCR5 expression was decreased in cultured B cells stimulated by BCR, CD40 ligands and IFN-β (p<0.05). By contrast, CXCR3 expression was increased in cultured B cells stimulated by BCR, CD40 ligands and IFN-γ (p<0.05). 4) T-bet expression was increased in cultured B cells stimulated by BCR, CD40 ligands and IFN-γ (p<0.05).

Conclusion: The results indicated that abnormality of B cell in SLE is characterized by not only quantitative increase in peripheral memory B cells but also unique expression pattern of chemokine receptors with down-regulation of CXCR5 and up-regulation of CXCR3 in EM B cells, indicating a potential of preferential migration into peripheral organs. Furthermore, in vitro experiments revealed that type I/II IFNs are a potent inducer of EM B cells involving abnormal chemokine receptor expression, suggesting an importance of these cytokines for the pathogenesis of SLE.


Disclosure: M. Yoshikawa, None; S. Nakayamada, None; S. Kubo, None; S. Iwata, None; K. Sakata, None; Y. Miyazaki, None; K. Nakano, None; K. Saito, None; Y. Tanaka, None.

To cite this abstract in AMA style:

Yoshikawa M, Nakayamada S, Kubo S, Iwata S, Sakata K, Miyazaki Y, Nakano K, Saito K, Tanaka Y. Type I/II Interferon Commits to Abnormal Expression of Chemokine Receptor on B Cells in Patients with Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/type-iii-interferon-commits-to-abnormal-expression-of-chemokine-receptor-on-b-cells-in-patients-with-systemic-lupus-erythematosus/. Accessed February 3, 2023.
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