The effect of Bat3/Tim-3 on IL-27/IL-10 expression in dendritic cells
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- 英文论文题名：The effect of Bat3/Tim-3 on IL-27/IL-10 expression in dendritic cells
- 论文作者：Gu Guangxiang ; Xia Qiang
- 英文论文作者：Gu Guangxiang ; Xia Qiang ; Department of Liver Surgery ; Renji Hospital ; Shanghai Jiaotong University School of Medicine
- 年：2016
- 作者机构：Department of Liver Surgery,Renji Hospital,Shanghai Jiaotong University School of Medicine;
- 英文论文关键词：Bat3 ; Tim-3 ; IL-27 ; IL-10
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R392
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：2
- 文件大小：1335k
- 原文格式：D
- 会议级别：全国
摘要
Purpose: To explore the effect of Bat3 on DCs and their function in immune tolerance induction, and further study the relationship between Bat3 and Tim-3 and possible mechanisms;Methods: First, we generated Bat3flox/flox CD11c-Cre+ mice. We generated bone marrow derived dendritic cells(BMDC). Then we tested their expression of co-stimulatory molecules, cytokine production and the function on T cells. To look at in vivo responses, we immunized the WT and Bat3 cko mice with MOG35-55/CFA plus PT, checked the behavioral changes.Next, we generated Bat3 Tim-3 double knockout mice to test whether the effect of Bat3 on DCs is independent of Tim-3 expression. Furthermore, we tested whether the effect of Bat3/Tim-3 on IL-27/IL-10 expression using a luciferase reporter assay and Chip-PCR.Results: Bat3 cko BM-DC expressed lower amounts of CD80, CD86 and MHC class II and secreted more IL-27 and IL-10 as checked by ELISA. Moreover, they could induce T cells to express more IL-10 in a co-culture experiment. When immunized with MOG35-55/CFA, Bat3 cko mice exhibited less severe disease. We found the effect of Tim-3 on DC to be opposite to that of Bat3 in the Tim-3cko mice. We also found the effect of Bat3 on DCs is dependent on Tim-3 by using Bat3 Tim-3 double knockout mice. At last, we found that Bat3 could inhibit IRF1-induced IL-27 and IL-10 expression as determined by a Luciferase Reporter Assay. The bindings of IRF1 to IL-27 and IL-10 promoter were enhanced in Bat3 cko BM-DC as we found using Chip-PCR. Co-IP experiments showed that Bat3 could bind to IRF1. Conclusion: Loss of Bat3 on DC could inhibit T cell response and EAE disease progression; Bat3 could bind to IRF1, and then suppress the IRF1 function, and further decrease IL-27 and IL-10 expression; The effect of Bat3 on DC is opposite to that of Tim-3, and its function is dependent on Tim-3 expression,
Purpose: To explore the effect of Bat3 on DCs and their function in immune tolerance induction, and further study the relationship between Bat3 and Tim-3 and possible mechanisms;Methods: First, we generated Bat3flox/flox CD11c-Cre+ mice. We generated bone marrow derived dendritic cells(BMDC). Then we tested their expression of co-stimulatory molecules, cytokine production and the function on T cells. To look at in vivo responses, we immunized the WT and Bat3 cko mice with MOG35-55/CFA plus PT, checked the behavioral changes.Next, we generated Bat3 Tim-3 double knockout mice to test whether the effect of Bat3 on DCs is independent of Tim-3 expression. Furthermore, we tested whether the effect of Bat3/Tim-3 on IL-27/IL-10 expression using a luciferase reporter assay and Chip-PCR.Results: Bat3 cko BM-DC expressed lower amounts of CD80, CD86 and MHC class II and secreted more IL-27 and IL-10 as checked by ELISA. Moreover, they could induce T cells to express more IL-10 in a co-culture experiment. When immunized with MOG35-55/CFA, Bat3 cko mice exhibited less severe disease. We found the effect of Tim-3 on DC to be opposite to that of Bat3 in the Tim-3cko mice. We also found the effect of Bat3 on DCs is dependent on Tim-3 by using Bat3 Tim-3 double knockout mice. At last, we found that Bat3 could inhibit IRF1-induced IL-27 and IL-10 expression as determined by a Luciferase Reporter Assay. The bindings of IRF1 to IL-27 and IL-10 promoter were enhanced in Bat3 cko BM-DC as we found using Chip-PCR. Co-IP experiments showed that Bat3 could bind to IRF1. Conclusion: Loss of Bat3 on DC could inhibit T cell response and EAE disease progression; Bat3 could bind to IRF1, and then suppress the IRF1 function, and further decrease IL-27 and IL-10 expression; The effect of Bat3 on DC is opposite to that of Tim-3, and its function is dependent on Tim-3 expression,
Purpose: To explore the effect of Bat3 on DCs and their function in immune tolerance induction, and further study the relationship between Bat3 and Tim-3 and possible mechanisms;Methods: First, we generated Bat3flox/flox CD11c-Cre+ mice. We generated bone marrow derived dendritic cells(BMDC). Then we tested their expression of co-stimulatory molecules, cytokine production and the function on T cells. To look at in vivo responses, we immunized the WT and Bat3 cko mice with MOG35-55/CFA plus PT, checked the behavioral changes.Next, we generated Bat3 Tim-3 double knockout mice to test whether the effect of Bat3 on DCs is independent of Tim-3 expression. Furthermore, we tested whether the effect of Bat3/Tim-3 on IL-27/IL-10 expression using a luciferase reporter assay and Chip-PCR.Results: Bat3 cko BM-DC expressed lower amounts of CD80, CD86 and MHC class II and secreted more IL-27 and IL-10 as checked by ELISA. Moreover, they could induce T cells to express more IL-10 in a co-culture experiment. When immunized with MOG35-55/CFA, Bat3 cko mice exhibited less severe disease. We found the effect of Tim-3 on DC to be opposite to that of Bat3 in the Tim-3cko mice. We also found the effect of Bat3 on DCs is dependent on Tim-3 by using Bat3 Tim-3 double knockout mice. At last, we found that Bat3 could inhibit IRF1-induced IL-27 and IL-10 expression as determined by a Luciferase Reporter Assay. The bindings of IRF1 to IL-27 and IL-10 promoter were enhanced in Bat3 cko BM-DC as we found using Chip-PCR. Co-IP experiments showed that Bat3 could bind to IRF1. Conclusion: Loss of Bat3 on DC could inhibit T cell response and EAE disease progression; Bat3 could bind to IRF1, and then suppress the IRF1 function, and further decrease IL-27 and IL-10 expression; The effect of Bat3 on DC is opposite to that of Tim-3, and its function is dependent on Tim-3 expression,
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