CD3+ B-1a Cells as a Mediator of Disease Progression in Autoimmune-Prone Mice
Joint Authors
Hirayama, Masahiro
Iwamoto, Shotaro
Yamamoto, Wakako
Toyoda, Hidemi
Xu, Dong-qing
Hanaki, Ryo
Morimoto, Mari
Nakato, Daisuke
Ito, Takahiro
Bonno, Motoki
Tanaka, Shigeki
Source
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-12-23
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
B-1a cells are distinguishable from conventional B cells, which are designated B-2 cells, on the basis of their developmental origin, surface marker expression, and functions.
In addition to the unique expression of the CD5 antigen, B-1a cells are characterized by the expression level of CD23.
Although B-1a cells are considered to be independent of T cells and produce natural autoantibodies that induce the clinical manifestations of autoimmune diseases, there is much debate on the role of B-1a cells in the development of autoimmune diseases.
We examined the involvement of B-1a cells in autoimmune-prone mice with the lpr gene.
MRL/lpr and B6/lpr mice exhibited lupus and lymphoproliferative syndromes because of the massive accumulation of CD3+CD4-CD8-B220+ T cells.
Interestingly, the B220+CD23-CD5+ (B-1a) cell population in the peripheral blood and peritoneal cavity increased with age and disease progression.
Ninety percent of B-1a cells were CD3 positive (CD3+ B-1a cells) and did not produce tumor necrosis factor alpha, interferon gamma, or interleukin-10.
To test the possible involvement of CD3+ B-1a cells in autoimmune disease, we tried to eliminate the peripheral cells by hypotonic shock through repeated intraperitoneal injections of distilled water.
The fraction of peritoneal CD3+ B-1a cells decreased, and symptoms of the autoimmune disease were much milder in the distilled water-treated MRL/lpr mice.
These results suggest that CD3+ B-1a cells could be mediators of disease progression in autoimmune-prone mice.
American Psychological Association (APA)
Yamamoto, Wakako& Toyoda, Hidemi& Xu, Dong-qing& Hanaki, Ryo& Morimoto, Mari& Nakato, Daisuke…[et al.]. 2018. CD3+ B-1a Cells as a Mediator of Disease Progression in Autoimmune-Prone Mice. Mediators of Inflammation،Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1204439
Modern Language Association (MLA)
Yamamoto, Wakako…[et al.]. CD3+ B-1a Cells as a Mediator of Disease Progression in Autoimmune-Prone Mice. Mediators of Inflammation No. 2018 (2018), pp.1-10.
https://search.emarefa.net/detail/BIM-1204439
American Medical Association (AMA)
Yamamoto, Wakako& Toyoda, Hidemi& Xu, Dong-qing& Hanaki, Ryo& Morimoto, Mari& Nakato, Daisuke…[et al.]. CD3+ B-1a Cells as a Mediator of Disease Progression in Autoimmune-Prone Mice. Mediators of Inflammation. 2018. Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1204439
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204439