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【bio-news】慢性胰腺炎症 to 1型糖尿病：B淋巴细胞
Objective: To determine the role of B cells in promoting CD8+ T cell-mediated β cell destruction in chronically inflamed islets.
Research Design and Methods: RIP-TNF-NOD mice were crossed to B cell deficient NOD mice and diabetes development monitored. In vitro antigen presentation assays, in vivo administration of the bromodeoxyuridine coupled to flow cytometry assays assessed intra-islet T cell activation in the absence or presence of B cells. CD4+Foxp3+ activity in the absence or presence of B cells was tested using in vivo depletion techniques. Cytokine production and apoptosis assays determined the capacity of CD8+ T cells transform to CTL and survive within inflamed islets in the absence or presence of B cells.
Results: B cell deficiency significantly delayed diabetes development in chronically inflamed islets. Re-introduction of B cells incapable of secreting Ig restored diabetes development. Both CD4+ and CD8+ T cell activation was unimpaired by B cell deficiency and delayed disease was not due to CD4+Foxp3+ T cell suppression of T cell responses. Instead at the CTL transition stage, B cell deficiency resulted in apoptosis of intra-islet CTL.
Conclusion: In inflamed islets, B cells are central for the efficient intra-islet survival of CTL thereby promoting type 1 diabetes development.
http://diabetes.diabetesjournals.org/cgi/content/abstract/db07-1256v1 B Cells Promote Intra-Islet CD8+ Cytotoxic T Lymphocyte Survival To Enhance Type 1 Diabetes
B细胞提高胰岛内CD8+细胞毒性T淋巴细胞生存率从而促进1型糖尿病发展
Objective: To determine the role of B cells in promoting CD8+ T cell-mediated β cell destruction in chronically inflamed islets.
目的：研究在慢性炎症胰岛，B细胞对CD8+T淋巴细胞介导的β细胞破坏影响。
Research Design and Methods: RIP-TNF-NOD mice were crossed to B cell deficient NOD mice and diabetes development monitored. In vitro antigen presentation assays, in vivo administration of the bromodeoxyuridine coupled to flow cytometry assays assessed intra-islet T cell activation in the absence or presence of B cells. CD4+Foxp3+ activity in the absence or presence of B cells was tested using in vivo depletion techniques. Cytokine production and apoptosis assays determined the capacity of CD8+ T cells transform to CTL and survive within inflamed islets in the absence or presence of B cells.
设计及方法：RIP-TNF-NOD小鼠与B细胞缺陷非肥胖糖尿病（NOD）小鼠交配获得子代，并且监测糖尿病病程发展。离体实验测定抗原呈递活性；在体动物实验，用溴脱氧尿苷处理后以流式细胞术检测B细胞（存在或不存在时）对胰岛内T细胞活性的影响。B细胞对CD4+Foxp3+活性的影响，采用小鼠体内耗竭B细胞技术检测。B细胞对CD8+T淋巴细胞的转化（转化为杀伤性T淋巴细胞（CTL））及存活能力的影响，通过相关细胞因子及细胞凋亡方法检测。
Results: B cell deficiency significantly delayed diabetes development in chronically inflamed islets. Re-introduction of B cells incapable of secreting Ig restored diabetes development. Both CD4+ and CD8+ T cell activation was unimpaired by B cell deficiency and delayed disease was not due to CD4+Foxp3+ T cell suppression of T cell responses. Instead at the CTL transition stage, B cell deficiency resulted in apoptosis of intra-islet CTL.
结果：在慢性炎症胰岛中，B细胞缺陷显著延缓糖尿病发展。补充B细胞(无Ig分泌能力)能恢复B细胞缺陷之前的促糖尿病发展作用。B细胞缺陷并不降低CD4+及CD8+ T淋巴细胞活性，并且慢性炎症的诱因不是T细胞应答引起的CD4+Foxp3+ T细胞活性降低。B细胞缺陷引起胰岛内CTL细胞凋亡但不影响CD8+T淋巴细胞向CTL转化。
Conclusion: In inflamed islets, B cells are central for the efficient intra-islet survival of CTL thereby promoting type 1 diabetes development.
结论：在炎症胰岛，B细胞对胰岛内CTL生存的起关键作用，这也是其促进1型糖尿病发展的原因。
编译：
B细胞提高胰岛内CD8+细胞毒性T淋巴细胞生存率从而促进1型糖尿病发展
目的：研究在慢性炎症胰岛，B细胞对CD8+T淋巴细胞介导的β细胞破坏影响。
设计及方法：RIP-TNF-NOD小鼠与B细胞缺陷非肥胖糖尿病（NOD）小鼠交配获得子代，并且监测糖尿病病程发展。离体实验测定抗原呈递活性；在体动物实验，用溴脱氧尿苷处理后以流式细胞术检测B细胞（存在或不存在时）对胰岛内T细胞活性的影响。B细胞对CD4+Foxp3+活性的影响，采用小鼠体内耗竭B细胞技术检测。B细胞对CD8+T淋巴细胞的转化（转化为杀伤性T淋巴细胞（CTL））及存活能力的影响，通过相关细胞因子及细胞凋亡方法检测。
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作者:admin@医学,生命科学 2011-08-22 06:39
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