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

Mediators of Inflammation

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

Diseases

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