Deficiency of beta-Arrestin 2 in Dendritic Cells Contributes to Autoimmune Diseases
文献类型:期刊论文
作者 | Cai, Yingying1; Yang, Cuixia1; Yu, Xiaohan2; Qian, Jie3; Dai, Min3; Wang, Yan4; Qin, Chaoyan1; Lai, Weiming1; Chen, Shuai1; Wang, Tingting1 |
刊名 | JOURNAL OF IMMUNOLOGY |
出版日期 | 2019-01-15 |
卷号 | 202期号:2页码:407-420 |
ISSN号 | 0022-1767 |
DOI | 10.4049/jimmunol.1800261 |
通讯作者 | Du, Changsheng(ducs2015@163.com) |
英文摘要 | Altered migration and immune responses of dendritic cells (DCs) lead to inflammatory and autoimmune diseases. Our studies demonstrated that beta-arrestin 2 deficiency promoted migration and cytokine production of mouse bone marrow-derived DCs. We further found that beta-arrestin 2 directly interacted with Zbtb46, a DC-specific transcription factor. What's more, our results suggested that the interaction between beta-arrestin 2 and Zbtb46 might negatively regulate DC migration. Using RNA sequencing, we indicated that genes CD74, NR4A1, and ZFP36 might be the target genes regulated by the interaction between beta-arrestin 2 and Zbtb46. Mice with selective deficiency of beta-arrestin 2 in DCs developed severer experimental autoimmune encephalomyelitis with more DC infiltration in the CNS and increased IL-6 in serum. In the systemic lupus erythematosus mice model, Arrb2(fl/fl) Itgax-cre(+) mice were prone to exacerbation of lupus nephritis with a higher level of IL-6 and DC accumulation. Taken together, our study identified beta-arrestin 2 as a new regulator of DC migration and immune properties, providing new insights into the mechanisms underlying the development of autoimmune disease. |
WOS关键词 | SYSTEMIC-LUPUS-ERYTHEMATOSUS ; COLLAGEN-INDUCED ARTHRITIS ; SIGNAL-TRANSDUCTION ; MULTIPLE-SCLEROSIS ; ADENOSINE RECEPTOR ; T-CELLS ; MIGRATION ; ACTIVATION ; BETA-ARRESTIN-2 ; ENDOCYTOSIS |
资助项目 | Ministry of Science and Technology of China[2014CB541903] ; National Natural Science Foundation of China[31871404] ; National Natural Science Foundation of China[31171348] ; Fundamental Research Funds for the Central Universities |
WOS研究方向 | Immunology |
语种 | 英语 |
出版者 | AMER ASSOC IMMUNOLOGISTS |
WOS记录号 | WOS:000455041800012 |
源URL | [http://119.78.100.183/handle/2S10ELR8/290849] |
专题 | 新药研究国家重点实验室 |
通讯作者 | Du, Changsheng |
作者单位 | 1.Tongji Univ, Shanghai Key Lab Signaling & Dis Res, Sch Life Sci & Technol, Putuo Dist Peoples Hosp, Shanghai 200092, Peoples R China 2.Yingshan Peoples Hosp, Dept Resp & Gastroenterol, Yingshan 436700, Hubei, Peoples R China 3.Shanghai Jiao Tong Univ, Renji Hosp, Sch Med, Shanghai 200001, Peoples R China 4.Shanghai Jiao Tong Univ, Chinese Acad Sci, Inst Hlth Sci, Shanghai Inst Biol Sci,Sch Med, Shanghai 200031, Peoples R China 5.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China |
推荐引用方式 GB/T 7714 | Cai, Yingying,Yang, Cuixia,Yu, Xiaohan,et al. Deficiency of beta-Arrestin 2 in Dendritic Cells Contributes to Autoimmune Diseases[J]. JOURNAL OF IMMUNOLOGY,2019,202(2):407-420. |
APA | Cai, Yingying.,Yang, Cuixia.,Yu, Xiaohan.,Qian, Jie.,Dai, Min.,...&Du, Changsheng.(2019).Deficiency of beta-Arrestin 2 in Dendritic Cells Contributes to Autoimmune Diseases.JOURNAL OF IMMUNOLOGY,202(2),407-420. |
MLA | Cai, Yingying,et al."Deficiency of beta-Arrestin 2 in Dendritic Cells Contributes to Autoimmune Diseases".JOURNAL OF IMMUNOLOGY 202.2(2019):407-420. |
入库方式: OAI收割
来源:上海药物研究所
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