Your browser doesn't support javascript.
loading
Antibody-mediated depletion of CCR10+EphA3+ cells ameliorates fibrosis in IPF.
Hohmann, Miriam S; Habiel, David M; Espindola, Milena S; Huang, Guanling; Jones, Isabelle; Narayanan, Rohan; Coelho, Ana Lucia; Oldham, Justin M; Noth, Imre; Ma, Shwu-Fan; Kurkciyan, Adrianne; McQualter, Jonathan L; Carraro, Gianni; Stripp, Barry; Chen, Peter; Jiang, Dianhua; Noble, Paul W; Parks, William; Woronicz, John; Yarranton, Geoffrey; Murray, Lynne A; Hogaboam, Cory M.
Afiliação
  • Hohmann MS; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Habiel DM; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Espindola MS; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Huang G; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Jones I; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Narayanan R; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Coelho AL; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Oldham JM; Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of California, Davis, Sacramento, California, USA.
  • Noth I; Division of Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine, University of Virginia, Charlottesville, Virginia, USA.
  • Ma SF; Division of Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine, University of Virginia, Charlottesville, Virginia, USA.
  • Kurkciyan A; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • McQualter JL; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Carraro G; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Stripp B; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Chen P; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Jiang D; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Noble PW; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Parks W; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
  • Woronicz J; KaloBios Pharmaceuticals, Inc. (now Humanigen, Inc.), Burlingame, California, USA.
  • Yarranton G; KaloBios Pharmaceuticals, Inc. (now Humanigen, Inc.), Burlingame, California, USA.
  • Murray LA; MiroBio Ltd, Oxford, United Kingdom.
  • Hogaboam CM; Women's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
JCI Insight ; 6(11)2021 06 08.
Article em En | MEDLINE | ID: mdl-33945505
Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant repair that diminishes lung function via mechanisms that remain poorly understood. CC chemokine receptor (CCR10) and its ligand CCL28 were both elevated in IPF compared with normal donors. CCR10 was highly expressed by various cells from IPF lungs, most notably stage-specific embryonic antigen-4-positive mesenchymal progenitor cells (MPCs). In vitro, CCL28 promoted the proliferation of CCR10+ MPCs while CRISPR/Cas9-mediated targeting of CCR10 resulted in the death of MPCs. Following the intravenous injection of various cells from IPF lungs into immunodeficient (NOD/SCID-γ, NSG) mice, human CCR10+ cells initiated and maintained fibrosis in NSG mice. Eph receptor A3 (EphA3) was among the highest expressed receptor tyrosine kinases detected on IPF CCR10+ cells. Ifabotuzumab-targeted killing of EphA3+ cells significantly reduced the numbers of CCR10+ cells and ameliorated pulmonary fibrosis in humanized NSG mice. Thus, human CCR10+ cells promote pulmonary fibrosis, and EphA3 mAb-directed elimination of these cells inhibits lung fibrosis.
Assuntos
Palavras-chave
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Receptor EphA3 / Receptores CCR10 / Fibrose Pulmonar Idiopática / Células-Tronco Mesenquimais Limite: Animals / Humans Idioma: En Revista: JCI Insight Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Estados Unidos
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Receptor EphA3 / Receptores CCR10 / Fibrose Pulmonar Idiopática / Células-Tronco Mesenquimais Limite: Animals / Humans Idioma: En Revista: JCI Insight Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Estados Unidos