title: Phenotypic and functional alterations of pDCs in lupus-prone mice.
abstract: Plasmacytoid dendritic cells (pDCs) were considered to be the major IFNα source in systemic lupus erythematosus (SLE) but their phenotype and function in different disease status have not been well studied. To study the function and phenotype of pDCs in lupus-prone mice we used 7 strains of lupus-prone mice including NZB/W F1, NZB, NZW, NZM2410, B6.NZM(Sle1/2/3), MRL/lpr and BXSB/Mp mice and C57BL/6 as control mice. Increased spleen pDC numbers were found in most lupus mice compared to C57BL/6 mice. The IFNα-producing ability of BM pDCs was similar between lupus and C57BL/6 mice, whereas pDCs from the spleens of NZB/W F1 and NZB mice produced more IFNα than pDCs from the spleens of C57BL/6 mice. Furthermore, spleen pDCs from MRL-lpr and NZM2410 mice showed increased responses to Tlr7 and Tlr9, respectively. As the disease progressed, IFN signature were evaluated in both BM and spleen pDC from lupus prone mice and the number of BM pDCs and their ability to produce IFNα gradually decreased in lupus-prone mice. In conclusion, pDC are activated alone with disease development and its phenotype and function differ among lupus-prone strains, and these differences may contribute to the development of lupus in these mice.
authors.affiliation: Shanghai Institute of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Zhenyuan
authors.initials: Z
authors.lastname: Zhou
authors.affiliation: Shanghai Institute of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Jianyang
authors.initials: J
authors.lastname: Ma
authors.affiliation: Shanghai Institute of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Chunyuan
authors.initials: C
authors.lastname: Xiao
authors.affiliation: Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS) &Shanghai Jiao Tong University School of Medicine (SJTUSM), Chinese Academy of Sciences (CAS), Shanghai, China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Han
authors.affiliation: Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS) &Shanghai Jiao Tong University School of Medicine (SJTUSM), Chinese Academy of Sciences (CAS), Shanghai, China.
authors.forename: Rong
authors.initials: R
authors.lastname: Qiu
authors.affiliation: Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS) &Shanghai Jiao Tong University School of Medicine (SJTUSM), Chinese Academy of Sciences (CAS), Shanghai, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Shanghai Institute of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Yingying
authors.initials: Y
authors.lastname: Zhou
authors.affiliation: Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University School of Medicine, Beijing, China.
authors.forename: Li
authors.initials: L
authors.lastname: Wu
authors.affiliation: Shanghai Institute of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Xinfang
authors.initials: X
authors.lastname: Huang
authors.affiliation: Shanghai Institute of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.|Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS) &Shanghai Jiao Tong University School of Medicine (SJTUSM), Chinese Academy of Sciences (CAS), Shanghai, China.|Division of Rheumatology and the Center for Autoimmune Genomics and Etiology (CAGE), Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
authors.forename: Nan
authors.initials: N
authors.lastname: Shen
mesh_terms: D000818:Animals; D002452:Cell Count; D002470:Cell Survival; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D016130:Immunophenotyping; D016898:Interferon-alpha / Q000096:biosynthesis; D008180:Lupus Erythematosus, Systemic / Q000175:diagnosis / Q000276:immunology* / Q000378:metabolism*; D008221:Lymphoid Tissue / Q000276:immunology / Q000378:metabolism; D051379:Mice; D019463:Mice, Inbred MRL lpr; D010641:Phenotype; D013154:Spleen / Q000276:immunology / Q000378:metabolism; D051199:Toll-Like Receptor 7 / Q000378:metabolism; D051217:Toll-Like Receptor 9 / Q000378:metabolism
chemical_list: D016898:Interferon-alpha; D051199:Toll-Like Receptor 7; D051217:Toll-Like Receptor 9