![](/images/graphics-bg.png)
CD38 Deficiency Downregulates the Onset and Pathogenesis of Collagen-Induced Arthritis through the NF-κB Pathway
المؤلفون المشاركون
Min, Weiping
Li, Qi
Liu, Zhenlong
Zhang, Huiqing
Du, Yuna
Song, Kuangyu
Li, Rong
Dai, Qianqian
Fu, Yingyuan
المصدر
Journal of Immunology Research
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-9، 9ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-03-05
دولة النشر
مصر
عدد الصفحات
9
التخصصات الرئيسية
الملخص EN
Aim.
The RelB gene plays an important role in guiding the progression of arthritis.
We have previously demonstrated that the expression of the RelB gene is decreased significantly in bone marrow DCs of CD38-/- mice.
In this study, we demonstrate that the cluster of the differentiation (CD38) gene could be a potentially therapeutic target for autoimmune arthritis.
Method.
Collagen-induced arthritis (CIA) models were generated with both the wild-type (WT) C57BL/6 and CD38-/- mice.
The expression of the RelB gene and maturation of bone marrow-derived dendritic cells (DCs) from the WT and CD38-/- mice were detected.
Antigen-specific T cell responses, joint damage, and expression of proinflammatory cytokines were assessed.
The effects of the Nuclear Factor Kappa B (NF-κB) transcription factor and its mechanisms were characterized.
Results.
We demonstrated that in CD38-/- mice, the expression of the RelB gene and major histocompatibility complex II (MHC II) was decreased, accompanied with the inhibited T cell reaction in a mixed lymphocyte reaction (MLR) in bone marrow-derived DCs.
Compared to the serious degeneration of the cartilage and the enlarged gap of the cavum articular in WT CIA mice, joint pathological changes of the CD38-/- CIA mice revealed marked attenuation, while the joint structures were well preserved.
The preserved effects were observed by the inhibition of proinflammatory cytokines and promotion of anti-inflammatory cytokines.
Furthermore, decreased phosphorylation of NF-κB was also observed in CD38-/- CIA mice.
Conclusion.
We demonstrate that CD38 could regulate CIA through NF-κB and this regulatory molecule could be a novel target for the treatment of autoimmune inflammatory joint disease.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Du, Yuna& Dai, Qianqian& Zhang, Huiqing& Li, Qi& Song, Kuangyu& Fu, Yingyuan…[et al.]. 2019. CD38 Deficiency Downregulates the Onset and Pathogenesis of Collagen-Induced Arthritis through the NF-κB Pathway. Journal of Immunology Research،Vol. 2019, no. 2019, pp.1-9.
https://search.emarefa.net/detail/BIM-1176611
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Du, Yuna…[et al.]. CD38 Deficiency Downregulates the Onset and Pathogenesis of Collagen-Induced Arthritis through the NF-κB Pathway. Journal of Immunology Research No. 2019 (2019), pp.1-9.
https://search.emarefa.net/detail/BIM-1176611
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Du, Yuna& Dai, Qianqian& Zhang, Huiqing& Li, Qi& Song, Kuangyu& Fu, Yingyuan…[et al.]. CD38 Deficiency Downregulates the Onset and Pathogenesis of Collagen-Induced Arthritis through the NF-κB Pathway. Journal of Immunology Research. 2019. Vol. 2019, no. 2019, pp.1-9.
https://search.emarefa.net/detail/BIM-1176611
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1176611
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
![](/images/ebook-kashef.png)
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
![](/images/kashef-image.png)