CD3+ B-1a Cells as a Mediator of Disease Progression in Autoimmune-Prone Mice
المؤلفون المشاركون
Hirayama, Masahiro
Iwamoto, Shotaro
Yamamoto, Wakako
Toyoda, Hidemi
Xu, Dong-qing
Hanaki, Ryo
Morimoto, Mari
Nakato, Daisuke
Ito, Takahiro
Bonno, Motoki
Tanaka, Shigeki
المصدر
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-12-23
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204439
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر