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  1. Article ; Online: Single-cell transcriptome analysis defines heterogeneity of the murine pancreatic ductal tree

    Audrey M Hendley / Arjun A Rao / Laura Leonhardt / Sudipta Ashe / Jennifer A Smith / Simone Giacometti / Xianlu L Peng / Honglin Jiang / David I Berrios / Mathias Pawlak / Lucia Y Li / Jonghyun Lee / Eric A Collisson / Mark S Anderson / Gabriela K Fragiadakis / Jen Jen Yeh / Chun Jimmie Ye / Grace E Kim / Valerie M Weaver /
    Matthias Hebrok

    eLife, Vol

    2021  Volume 10

    Abstract: To study disease development, an inventory of an organ's cell types and understanding of physiologic function is paramount. Here, we performed single-cell RNA-sequencing to examine heterogeneity of murine pancreatic duct cells, pancreatobiliary cells, ... ...

    Abstract To study disease development, an inventory of an organ's cell types and understanding of physiologic function is paramount. Here, we performed single-cell RNA-sequencing to examine heterogeneity of murine pancreatic duct cells, pancreatobiliary cells, and intrapancreatic bile duct cells. We describe an epithelial-mesenchymal transitory axis in our three pancreatic duct subpopulations and identify osteopontin as a regulator of this fate decision as well as human duct cell dedifferentiation. Our results further identify functional heterogeneity within pancreatic duct subpopulations by elucidating a role for geminin in accumulation of DNA damage in the setting of chronic pancreatitis. Our findings implicate diverse functional roles for subpopulations of pancreatic duct cells in maintenance of duct cell identity and disease progression and establish a comprehensive road map of murine pancreatic duct cell, pancreatobiliary cell, and intrapancreatic bile duct cell homeostasis.
    Keywords scRNA-seq ; pancreatic duct ligation ; Osteopontin ; Geminin ; duct heterogeneity ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-05-01T00:00:00Z
    Publisher eLife Sciences Publications Ltd
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: RBPJ Controls Development of Pathogenic Th17 Cells by Regulating IL-23 Receptor Expression

    Gerd Meyer zu Horste / Chuan Wu / Chao Wang / Le Cong / Mathias Pawlak / Youjin Lee / Wassim Elyaman / Sheng Xiao / Aviv Regev / Vijay K. Kuchroo

    Cell Reports, Vol 16, Iss 2, Pp 392-

    2016  Volume 404

    Abstract: Interleukin-17 (IL-17)-producing helper T cells (Th17 cells) play an important role in autoimmune diseases. However, not all Th17 cells induce tissue inflammation or autoimmunity. Th17 cells require IL-23 receptor (IL-23R) signaling to become pathogenic. ...

    Abstract Interleukin-17 (IL-17)-producing helper T cells (Th17 cells) play an important role in autoimmune diseases. However, not all Th17 cells induce tissue inflammation or autoimmunity. Th17 cells require IL-23 receptor (IL-23R) signaling to become pathogenic. The transcriptional mechanisms controlling the pathogenicity of Th17 cells and IL-23R expression are unknown. Here, we demonstrate that the canonical Notch signaling mediator RBPJ is a key driver of IL-23R expression. In the absence of RBPJ, Th17 cells fail to upregulate IL-23R, lack stability, and do not induce autoimmune tissue inflammation in vivo, whereas overexpression of IL-23R rescues this defect and promotes pathogenicity of RBPJ-deficient Th17 cells. RBPJ binds and trans-activates the Il23r promoter and induces IL-23R expression and represses anti-inflammatory IL-10 production in Th17 cells. We thus find that Notch signaling influences the development of pathogenic and non-pathogenic Th17 cells by reciprocally regulating IL-23R and IL-10 expression.
    Keywords Th17 cells ; pathogenicity ; IL-23R ; RBPJ ; Notch ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2016-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article: CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity

    Wang, Chao / Nir Yosef / Jellert Gaublomme / Chuan Wu / Youjin Lee / Clary B. Clish / Jim Kaminski / Sheng Xiao / Gerd Meyer Zu Horste / Mathias Pawlak / Yasuhiro Kishi / Nicole Joller / Katarzyna Karwacz / Chen Zhu / Maria Ordovas-Montanes / Asaf Madi / Ivo Wortman / Toru Miyazaki / Raymond A. Sobel /
    Hongkun Park / Aviv Regev / Vijay K. Kuchroo

    Cell. 2015 Dec. 03, v. 163

    2015  

    Abstract: Th17 cells play a critical role in host defense against extracellular pathogens and tissue homeostasis but can induce autoimmunity. The mechanisms implicated in balancing “pathogenic” and “non-pathogenic” Th17 cell states remain largely unknown. ... ...

    Abstract Th17 cells play a critical role in host defense against extracellular pathogens and tissue homeostasis but can induce autoimmunity. The mechanisms implicated in balancing “pathogenic” and “non-pathogenic” Th17 cell states remain largely unknown. We used single-cell RNA-seq to identify CD5L/AIM as a regulator expressed in non-pathogenic, but not in pathogenic Th17 cells. Although CD5L does not affect Th17 differentiation, it is a functional switch that regulates the pathogenicity of Th17 cells. Loss of CD5L converts non-pathogenic Th17 cells into pathogenic cells that induce autoimmunity. CD5L mediates this effect by modulating the intracellular lipidome, altering fatty acid composition and restricting cholesterol biosynthesis and, thus, ligand availability for Rorγt, the master transcription factor of Th17 cells. Our study identifies CD5L as a critical regulator of the Th17 cell functional state and highlights the importance of lipid metabolism in balancing immune protection and disease induced by T cells.
    Keywords T-lymphocytes ; autoimmunity ; biosynthesis ; cholesterol ; fatty acid composition ; homeostasis ; ligands ; lipid metabolism ; pathogenicity ; pathogens ; sequence analysis ; transcription factors
    Language English
    Dates of publication 2015-1203
    Size p. 1413-1427.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2015.10.068
    Database NAL-Catalogue (AGRICOLA)

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