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Abstract Number: 0836

SH3BP2 Deficiency Ameliorates Murine Systemic Lupus Erythematosus

Tomoyuki Mukai1, Kyoko Kawahara1, Masanori Iseki2, Akiko Nagasu1, Hajime Nagasu3, Takahiko Akagi1, Shoko Tsuji1, Yasuyoshi Ueki4, Katsuhiko Ishihara2, Naoki Kashihara3 and Yoshitaka Morita1, 1Department of Rheumatology, Kawasaki Medical School, Kurashiki, Okayama, Japan, 2Department of Immunology and Molecular Genetics, Kawasaki Medical School, Kurashiki, Okayama, Japan, 3Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan, 4Department of Biomedical Sciences and Comprehensive Care, Indiana University School of Dentistry, Indianapolis, IN

Meeting: ACR Convergence 2020

Keywords: Animal Model, Systemic lupus erythematosus (SLE)

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Session Information

Date: Saturday, November 7, 2020

Session Title: SLE – Animal Models Poster

Session Type: Poster Session B

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

Background/Purpose: The adaptor protein, Src homology 3 domain-binding protein 2 (SH3BP2), is widely expressed in immune cells, such as myeloid cells, B cells, and T cells. It controls intracellular signaling pathways such as Syk and Src. The present study was undertaken to investigate the role of SH3BP2 in a murine systemic lupus erythematosus model and to explore differential phenotypes in immune cell sub-populations isolated from SH3BP2-deficient mice.

Methods: For the lupus model, we used Faslpr mice (C57BL/6 background). Clinical and immunological phenotypes were compared between Faslpr and SH3BP2-deficient Faslpr mice. Splenomegaly and renal involvement were assessed in 35-week-old mice. Serum levels of anti-dsDNA antibody and rheumatoid factor were determined using ELISA. Lymphocyte subsets in spleen and lymph nodes were analyzed by flow cytometry. To examine the role of SH3BP2 in specific cells, B cell-specific SH3BP2-deficient lupus mice were generated and analyzed; differentiation of bone marrow-derived dendritic cell and activation of T cells and macrophages were determined in vitro.

Results: SH3BP2 deficiency significantly reduced lupus-like phenotypes, such as splenomegaly, renal involvement, elevated serum dsDNA antibody and rheumatoid factor, and increased splenic B220+CD4–CD8– T cells. Notably, SH3BP2 deficiency in B cells did not rescue the lupus-like phenotypes. Interestingly, SH3BP2 deficiency suppressed the differentiation of dendritic cells but it did not affect the functions of T cells and macrophages in vitro.

Conclusion: SH3BP2 deficiency ameliorated clinical and immunological manifestations in lupus-prone mice, possibly via targeting dendritic cells differentiation. Modulating SH3BP2 expression could thus provide a novel therapeutic approach to autoimmune diseases.


Disclosure: T. Mukai, Chugai Pharmaceutical Co., 2, AYUMI Pharmaceutical Co., 2; K. Kawahara, Chugai Pharmaceutical Co., 2, AYUMI Pharmaceutical Co., 2; M. Iseki, None; A. Nagasu, Chugai Pharmaceutical Co., 2, AYUMI Pharmaceutical Co., 2; H. Nagasu, None; T. Akagi, Chugai Pharmaceutical Co., 2, AYUMI Pharmaceutical Co., 2; S. Tsuji, Chugai Pharmaceutical Co., 2, AYUMI Pharmaceutical Co., 2; Y. Ueki, None; K. Ishihara, None; N. Kashihara, None; Y. Morita, Chugai Pharmaceutical Co., 2, AYUMI Pharmaceutical Co., 2.

To cite this abstract in AMA style:

Mukai T, Kawahara K, Iseki M, Nagasu A, Nagasu H, Akagi T, Tsuji S, Ueki Y, Ishihara K, Kashihara N, Morita Y. SH3BP2 Deficiency Ameliorates Murine Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2020; 72 (suppl 10). https://acrabstracts.org/abstract/sh3bp2-deficiency-ameliorates-murine-systemic-lupus-erythematosus/. Accessed January 20, 2021.
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