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  1. Article ; Online: Positive selection of IgG

    Sundling, Christopher / Lau, Angelica W Y / Bourne, Katherine / Young, Clara / Laurianto, Candy / Hermes, Jana R / Menzies, Rosemary J / Butt, Danyal / Kräutler, Nike J / Zahra, David / Suan, Dan / Brink, Robert

    Immunity

    2021  Volume 54, Issue 5, Page(s) 988–1001.e5

    Abstract: Positive selection of high-affinity B cells within germinal centers (GCs) drives affinity maturation of antibody responses. Here, we examined the mechanism underlying the parallel transition from immunoglobulin M (IgM) to IgG. Early GCs contained mostly ... ...

    Abstract Positive selection of high-affinity B cells within germinal centers (GCs) drives affinity maturation of antibody responses. Here, we examined the mechanism underlying the parallel transition from immunoglobulin M (IgM) to IgG. Early GCs contained mostly unswitched IgM
    MeSH term(s) Animals ; Antibody Formation/immunology ; Antigens/immunology ; B-Lymphocytes/immunology ; Female ; Germinal Center/immunology ; Immunoglobulin Class Switching/immunology ; Immunoglobulin G/immunology ; Immunoglobulin M/immunology ; Immunoglobulin Variable Region/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Sheep/immunology ; Somatic Hypermutation, Immunoglobulin/immunology
    Chemical Substances Antigens ; Immunoglobulin G ; Immunoglobulin M ; Immunoglobulin Variable Region
    Language English
    Publishing date 2021-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2021.03.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: IL11-mediated stromal cell activation may not be the master regulator of pro-fibrotic signaling downstream of TGFβ.

    Tan, Yunhao / Mosallanejad, Kenta / Zhang, Qingxiu / O'Brien, Stephen / Clements, Meghan / Perper, Stuart / Wilson, Sarah / Chaulagain, Sudiksha / Wang, Jing / Abdalla, Mary / Al-Saidi, Helen / Butt, Danyal / Clabbers, Anca / Ofori, Kwasi / Dillon, Beth / Harvey, Bohdan / Memmott, John / Negron, Christopher / Winarta, David /
    Tan, Catherine / Biswas, Amlan / Dong, Feng / Morales-Tirado, Vanessa / Lu, Xiaoqing / Singh, Gurminder / White, Michael / Ashley, Shanna / Knight, Heather / Westmoreland, Susan / Phillips, Lucy / Carr, Tracy / Reinke-Breen, Lauren / Singh, Rajeeva / Xu, Jianwen / Wu, Kan / Rinaldi, Lisa / Stoll, Brian / He, Yupeng David / Hazelwood, Lisa / Karman, Jozsef / McCluskey, Andrew / Stine, William / Correia, Ivan / Gauld, Stephen / Levesque, Marc C / Veldman, Geertruida / Hubeau, Cedric / Radstake, Timothy / Sadhukhan, Ramkrishna / Fiebiger, Edda

    Frontiers in immunology

    2024  Volume 15, Page(s) 1293883

    Abstract: Fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF) and systemic scleroderma (SSc), are commonly associated with high morbidity and mortality, thereby representing a significant unmet medical need. Interleukin 11 (IL11)-mediated cell ... ...

    Abstract Fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF) and systemic scleroderma (SSc), are commonly associated with high morbidity and mortality, thereby representing a significant unmet medical need. Interleukin 11 (IL11)-mediated cell activation has been identified as a central mechanism for promoting fibrosis downstream of TGFβ. IL11 signaling has recently been reported to promote fibroblast-to-myofibroblast transition, thus leading to various pro-fibrotic phenotypic changes. We confirmed increased mRNA expression of IL11 and IL11Rα in fibrotic diseases by OMICs approaches and
    MeSH term(s) Humans ; Transforming Growth Factor beta/metabolism ; Interleukin-11 ; Signal Transduction ; Fibrosis ; Myofibroblasts/metabolism
    Chemical Substances Transforming Growth Factor beta ; Interleukin-11
    Language English
    Publishing date 2024-02-22
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1293883
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: An anti-TL1A antibody for the treatment of asthma and inflammatory bowel disease.

    Clarke, Adam W / Poulton, Lynn / Shim, Doris / Mabon, David / Butt, Danyal / Pollard, Matthew / Pande, Vanya / Husten, Jean / Lyons, Jacquelyn / Tian, Chen / Doyle, Anthony G

    mAbs

    2018  Volume 10, Issue 4, Page(s) 664–677

    Abstract: TL1A is an attractive therapeutic target for the treatment of mucosal inflammation associated with inflammatory bowel disease (IBD) and asthma. Blockade of the TL1A pathway has been shown to reduce inflammatory responses while leaving baseline immunity ... ...

    Abstract TL1A is an attractive therapeutic target for the treatment of mucosal inflammation associated with inflammatory bowel disease (IBD) and asthma. Blockade of the TL1A pathway has been shown to reduce inflammatory responses while leaving baseline immunity intact, and to be beneficial in animal models of colitis and asthma. Given the therapeutic potential of blocking this pathway in IBD and asthma, we developed C03V, a human antibody that binds with high affinity to soluble and membrane-bound TL1A. In an assay measuring apoptosis induced by exogenous TL1A, C03V was 43-fold more potent than the next most potent anti-TL1A antibody analyzed. C03V also potently inhibited endogenous TL1A activity in a primary cell-based assay. This potency was linked to the C03V-binding epitope on TL1A, encompassing the residue R32. This residue is critical for the binding of TL1A to its signaling receptor DR3 but not to its decoy receptor DcR3, and explains why C03V inhibited TL1A-DR3 binding to a much greater extent than TL1A-DcR3 binding. This characteristic may be advantageous to preserve some of the homeostatic functions of DcR3, such as TL1A antagonism. In colitis models, C03V significantly ameliorated microscopic, macroscopic and clinical aspects of disease pathology, and in an asthma model it significantly reduced airways inflammation. Notable in both types of disease model was the reduction in fibrosis observed after C03V treatment. C03V has the potential to address unmet medical needs in asthma and IBD.
    MeSH term(s) Animals ; Antibodies, Monoclonal/chemistry ; Antibodies, Monoclonal/pharmacology ; Asthma/immunology ; Humans ; Inflammatory Bowel Diseases/immunology ; Tumor Necrosis Factor Ligand Superfamily Member 15/antagonists & inhibitors
    Chemical Substances Antibodies, Monoclonal ; TNFSF15 protein, human ; Tumor Necrosis Factor Ligand Superfamily Member 15
    Language English
    Publishing date 2018-03-05
    Publishing country United States
    Document type Journal Article
    ISSN 1942-0870
    ISSN (online) 1942-0870
    DOI 10.1080/19420862.2018.1440164
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: CCR6 Defines Memory B Cell Precursors in Mouse and Human Germinal Centers, Revealing Light-Zone Location and Predominant Low Antigen Affinity.

    Suan, Dan / Kräutler, Nike J / Maag, Jesper L V / Butt, Danyal / Bourne, Katherine / Hermes, Jana R / Avery, Danielle T / Young, Clara / Statham, Aaron / Elliott, Michael / Dinger, Marcel E / Basten, Antony / Tangye, Stuart G / Brink, Robert

    Immunity

    2017  Volume 47, Issue 6, Page(s) 1142–1153.e4

    Abstract: Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC ...

    Abstract Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC differentiation, no such marker exists for cells committed to the MBC lineage. Here, we report that the chemokine receptor CCR6 uniquely marks MBC precursors in both mouse and human GCs. CCR6
    MeSH term(s) Animals ; B7-2 Antigen/genetics ; B7-2 Antigen/immunology ; Cell Differentiation ; Cell Lineage/immunology ; Gene Expression Profiling ; Gene Expression Regulation ; Germinal Center/cytology ; Germinal Center/immunology ; Humans ; Immunity, Humoral ; Immunologic Memory ; Immunophenotyping ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Phenotype ; Plasma Cells/cytology ; Plasma Cells/immunology ; Positive Regulatory Domain I-Binding Factor 1/genetics ; Positive Regulatory Domain I-Binding Factor 1/immunology ; Precursor Cells, B-Lymphoid/cytology ; Precursor Cells, B-Lymphoid/immunology ; Receptors, CCR6/genetics ; Receptors, CCR6/immunology ; Receptors, CXCR4/genetics ; Receptors, CXCR4/immunology ; Signal Transduction
    Chemical Substances B7-2 Antigen ; CCR6 protein, mouse ; CXCR4 protein, mouse ; Cd86 protein, mouse ; Prdm1 protein, mouse ; Receptors, CCR6 ; Receptors, CXCR4 ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-)
    Language English
    Publishing date 2017--19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2017.11.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Differentiation of germinal center B cells into plasma cells is initiated by high-affinity antigen and completed by Tfh cells.

    Kräutler, Nike J / Suan, Dan / Butt, Danyal / Bourne, Katherine / Hermes, Jana R / Chan, Tyani D / Sundling, Christopher / Kaplan, Warren / Schofield, Peter / Jackson, Jennifer / Basten, Antony / Christ, Daniel / Brink, Robert

    The Journal of experimental medicine

    2017  Volume 214, Issue 5, Page(s) 1259–1267

    Abstract: Plasma cells (PCs) derived from germinal centers (GCs) secrete the high-affinity antibodies required for long-term serological immunity. Nevertheless, the process whereby GC B cells differentiate into PCs is uncharacterized, and the mechanism underlying ... ...

    Abstract Plasma cells (PCs) derived from germinal centers (GCs) secrete the high-affinity antibodies required for long-term serological immunity. Nevertheless, the process whereby GC B cells differentiate into PCs is uncharacterized, and the mechanism underlying the selective PC differentiation of only high-affinity GC B cells remains unknown. In this study, we show that differentiation into PCs is induced among a discrete subset of high-affinity B cells residing within the light zone of the GC. Initiation of differentiation required signals delivered upon engagement with intact antigen. Signals delivered by T follicular helper cells were not required to initiate differentiation but were essential to complete the differentiation process and drive migration of maturing PCs through the dark zone and out of the GC. This bipartite or two-signal mechanism has likely evolved to both sustain protective immunity and avoid autoantibody production.
    MeSH term(s) Animals ; Antigens, Differentiation, B-Lymphocyte/physiology ; B-Lymphocytes/physiology ; Cell Differentiation/physiology ; Germinal Center/physiology ; Mice ; Mice, Inbred C57BL ; Plasma Cells/physiology ; T-Lymphocytes, Helper-Inducer/physiology
    Chemical Substances Antigens, Differentiation, B-Lymphocyte
    Language English
    Publishing date 2017-03-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20161533
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Elimination of germinal-center-derived self-reactive B cells is governed by the location and concentration of self-antigen.

    Chan, Tyani D / Wood, Katherine / Hermes, Jana R / Butt, Danyal / Jolly, Christopher J / Basten, Antony / Brink, Robert

    Immunity

    2012  Volume 37, Issue 5, Page(s) 893–904

    Abstract: Secondary diversification of the B cell repertoire by immunoglobulin gene somatic hypermutation in the germinal center (GC) is essential for providing the high-affinity antibody specificities required for long-term humoral immunity. While the risk to ... ...

    Abstract Secondary diversification of the B cell repertoire by immunoglobulin gene somatic hypermutation in the germinal center (GC) is essential for providing the high-affinity antibody specificities required for long-term humoral immunity. While the risk to self-tolerance posed by inadvertent generation of self-reactive GC B cells has long been recognized, it has not previously been possible to identify such cells and study their fate. In the current study, self-reactive B cells generated de novo in the GC failed to survive when their target self-antigen was either expressed ubiquitously or specifically in cells proximal to the GC microenvironment. By contrast, GC B cells that recognized rare or tissue-specific self-antigens were not eliminated, and could instead undergo positive selection by cross-reactive foreign antigen and produce plasma cells secreting high-affinity autoantibodies. These findings demonstrate the incomplete nature of GC self-tolerance and may explain the frequent association of cross-reactive, organ-specific autoantibodies with postinfectious autoimmune disease.
    MeSH term(s) Animals ; Antibody Affinity/genetics ; Antibody Affinity/immunology ; Autoantigens/genetics ; Autoantigens/immunology ; Autoantigens/metabolism ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; CHO Cells ; Cell Line ; Cellular Microenvironment/genetics ; Cellular Microenvironment/immunology ; Cricetinae ; Cross Reactions ; Genes, Immunoglobulin ; Germinal Center/immunology ; Germinal Center/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Plasma Cells/immunology ; Plasma Cells/metabolism ; Somatic Hypermutation, Immunoglobulin/genetics ; Somatic Hypermutation, Immunoglobulin/immunology
    Chemical Substances Autoantigens
    Language English
    Publishing date 2012-11-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2012.07.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Memory B cells are reactivated in subcapsular proliferative foci of lymph nodes.

    Moran, Imogen / Nguyen, Akira / Khoo, Weng Hua / Butt, Danyal / Bourne, Katherine / Young, Clara / Hermes, Jana R / Biro, Maté / Gracie, Gary / Ma, Cindy S / Munier, C Mee Ling / Luciani, Fabio / Zaunders, John / Parker, Andrew / Kelleher, Anthony D / Tangye, Stuart G / Croucher, Peter I / Brink, Robert / Read, Mark N /
    Phan, Tri Giang

    Nature communications

    2018  Volume 9, Issue 1, Page(s) 3372

    Abstract: Vaccine-induced immunity depends on the generation of memory B cells (MBC). However, where and how MBCs are reactivated to make neutralising antibodies remain unknown. Here we show that MBCs are prepositioned in a subcapsular niche in lymph nodes where, ... ...

    Abstract Vaccine-induced immunity depends on the generation of memory B cells (MBC). However, where and how MBCs are reactivated to make neutralising antibodies remain unknown. Here we show that MBCs are prepositioned in a subcapsular niche in lymph nodes where, upon reactivation by antigen, they rapidly proliferate and differentiate into antibody-secreting plasma cells in the subcapsular proliferative foci (SPF). This novel structure is enriched for signals provided by T follicular helper cells and antigen-presenting subcapsular sinus macrophages. Compared with contemporaneous secondary germinal centres, SPF have distinct single-cell molecular signature, cell migration pattern and plasma cell output. Moreover, SPF are found both in human and mouse lymph nodes, suggesting that they are conserved throughout mammalian evolution. Our data thus reveal that SPF is a seat of immunological memory that may be exploited to rapidly mobilise secondary antibody responses and improve vaccine efficacy.
    MeSH term(s) Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/metabolism ; Cell Movement/drug effects ; Cells, Cultured ; Flow Cytometry ; Humans ; Lymph Nodes/immunology ; Lymph Nodes/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Theoretical ; Pyrazoles/pharmacology ; Pyrimidines/pharmacology ; Tamoxifen/pharmacology
    Chemical Substances Pyrazoles ; Pyrimidines ; Tamoxifen (094ZI81Y45) ; ibrutinib (1X70OSD4VX)
    Language English
    Publishing date 2018-08-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-018-05772-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: FAS Inactivation Releases Unconventional Germinal Center B Cells that Escape Antigen Control and Drive IgE and Autoantibody Production.

    Butt, Danyal / Chan, Tyani D / Bourne, Katherine / Hermes, Jana R / Nguyen, Akira / Statham, Aaron / O'Reilly, Lorraine A / Strasser, Andreas / Price, Susan / Schofield, Peter / Christ, Daniel / Basten, Antony / Ma, Cindy S / Tangye, Stuart G / Phan, Tri Giang / Rao, V Koneti / Brink, Robert

    Immunity

    2015  Volume 42, Issue 5, Page(s) 890–902

    Abstract: The mechanistic links between genetic variation and autoantibody production in autoimmune disease remain obscure. Autoimmune lymphoproliferative syndrome (ALPS) is caused by inactivating mutations in FAS or FASL, with autoantibodies thought to arise ... ...

    Abstract The mechanistic links between genetic variation and autoantibody production in autoimmune disease remain obscure. Autoimmune lymphoproliferative syndrome (ALPS) is caused by inactivating mutations in FAS or FASL, with autoantibodies thought to arise through failure of FAS-mediated removal of self-reactive germinal center (GC) B cells. Here we show that FAS is in fact not required for this process. Instead, FAS inactivation led to accumulation of a population of unconventional GC B cells that underwent somatic hypermutation, survived despite losing antigen reactivity, and differentiated into a large population of plasma cells that included autoantibody-secreting clones. IgE(+) plasma cell numbers, in particular, increased after FAS inactivation and a major cohort of ALPS-affected patients were found to have hyper-IgE. We propose that these previously unidentified cells, designated "rogue GC B cells," are a major driver of autoantibody production and provide a mechanistic explanation for the linked production of IgE and autoantibodies in autoimmune disease.
    MeSH term(s) Animals ; Autoantibodies/biosynthesis ; Autoantibodies/immunology ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Fluorescent Antibody Technique ; Germinal Center/cytology ; Germinal Center/immunology ; Humans ; Immunoglobulin E/biosynthesis ; Immunoglobulin E/immunology ; Mice ; Polymerase Chain Reaction ; fas Receptor/deficiency ; fas Receptor/immunology ; fas Receptor/metabolism
    Chemical Substances Autoantibodies ; fas Receptor ; Immunoglobulin E (37341-29-0)
    Language English
    Publishing date 2015-05-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2015.04.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Osteoclasts recycle via osteomorphs during RANKL-stimulated bone resorption.

    McDonald, Michelle M / Khoo, Weng Hua / Ng, Pei Ying / Xiao, Ya / Zamerli, Jad / Thatcher, Peter / Kyaw, Wunna / Pathmanandavel, Karrnan / Grootveld, Abigail K / Moran, Imogen / Butt, Danyal / Nguyen, Akira / Corr, Alexander / Warren, Sean / Biro, Maté / Butterfield, Natalie C / Guilfoyle, Siobhan E / Komla-Ebri, Davide / Dack, Michael R G /
    Dewhurst, Hannah F / Logan, John G / Li, Yongxiao / Mohanty, Sindhu T / Byrne, Niall / Terry, Rachael L / Simic, Marija K / Chai, Ryan / Quinn, Julian M W / Youlten, Scott E / Pettitt, Jessica A / Abi-Hanna, David / Jain, Rohit / Weninger, Wolfgang / Lundberg, Mischa / Sun, Shuting / Ebetino, Frank H / Timpson, Paul / Lee, Woei Ming / Baldock, Paul A / Rogers, Michael J / Brink, Robert / Williams, Graham R / Bassett, J H Duncan / Kemp, John P / Pavlos, Nathan J / Croucher, Peter I / Phan, Tri Giang

    Cell

    2021  Volume 184, Issue 5, Page(s) 1330–1347.e13

    Abstract: Osteoclasts are large multinucleated bone-resorbing cells formed by the fusion of monocyte/macrophage-derived precursors that are thought to undergo apoptosis once resorption is complete. Here, by intravital imaging, we reveal that RANKL-stimulated ... ...

    Abstract Osteoclasts are large multinucleated bone-resorbing cells formed by the fusion of monocyte/macrophage-derived precursors that are thought to undergo apoptosis once resorption is complete. Here, by intravital imaging, we reveal that RANKL-stimulated osteoclasts have an alternative cell fate in which they fission into daughter cells called osteomorphs. Inhibiting RANKL blocked this cellular recycling and resulted in osteomorph accumulation. Single-cell RNA sequencing showed that osteomorphs are transcriptionally distinct from osteoclasts and macrophages and express a number of non-canonical osteoclast genes that are associated with structural and functional bone phenotypes when deleted in mice. Furthermore, genetic variation in human orthologs of osteomorph genes causes monogenic skeletal disorders and associates with bone mineral density, a polygenetic skeletal trait. Thus, osteoclasts recycle via osteomorphs, a cell type involved in the regulation of bone resorption that may be targeted for the treatment of skeletal diseases.
    MeSH term(s) Animals ; Apoptosis ; Bone Resorption/metabolism ; Bone Resorption/pathology ; Cell Fusion ; Cells, Cultured ; Humans ; Macrophages/cytology ; Mice ; Osteochondrodysplasias/drug therapy ; Osteochondrodysplasias/genetics ; Osteochondrodysplasias/metabolism ; Osteochondrodysplasias/pathology ; Osteoclasts/metabolism ; Osteoclasts/pathology ; RANK Ligand/metabolism ; Signal Transduction
    Chemical Substances RANK Ligand ; Tnfsf11 protein, mouse
    Language English
    Publishing date 2021-02-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2021.02.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Osteoclasts recycle via osteomorphs during RANKL-stimulated bone resorption.

    McDonald, Michelle M / Khoo, Weng Hua / Ng, Pei Ying / Xiao, Ya / Zamerli, Jad / Thatcher, Peter / Kyaw, Wunna / Pathmanandavel, Karrnan / Grootveld, Abigail K / Moran, Imogen / Butt, Danyal / Nguyen, Akira / Corr, Alexander / Warren, Sean / Biro, Maté / Butterfield, Natalie C / Guilfoyle, Siobhan E / Komla-Ebri, Davide / Dack, Michael R G /
    Dewhurst, Hannah F / Logan, John G / Li, Yongxiao / Mohanty, Sindhu T / Byrne, Niall / Terry, Rachael L / Simic, Marija K / Chai, Ryan / Quinn, Julian M W / Youlten, Scott E / Pettitt, Jessica A / Abi-Hanna, David / Jain, Rohit / Weninger, Wolfgang / Lundberg, Mischa / Sun, Shuting / Ebetino, Frank H / Timpson, Paul / Lee, Woei Ming / Baldock, Paul A / Rogers, Michael J / Brink, Robert / Williams, Graham R / Bassett, J H Duncan / Kemp, John P / Pavlos, Nathan J / Croucher, Peter I / Phan, Tri Giang

    Cell

    2021  Volume 184, Issue 7, Page(s) 1940

    Language English
    Publishing date 2021-03-08
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2021.03.010
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