Cardiac fibroblasts mediate IL-17A–driven inflammatory dilated cardiomyopathy

IL-17A stimulates cardiac fibroblasts to produce inflammatory mediators critical for the recruitment and differentiation of myeloid cells during inflammatory dilated cardiomyopathy.

[1]  Ansuman T. Satpathy,et al.  Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation. , 2014, Immunity.

[2]  A. Ashare,et al.  Low Levels of Insulin-like Growth Factor-1 Contribute to Alveolar Macrophage Dysfunction in Cystic Fibrosis , 2013, The Journal of Immunology.

[3]  M. Cybulsky,et al.  Faculty Opinions recommendation of Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes. , 2013 .

[4]  Thomas A. Wynn,et al.  Macrophage biology in development, homeostasis and disease , 2013, Nature.

[5]  U. Eriksson,et al.  GM-CSF promotes inflammatory dendritic cell formation but does not contribute to disease progression in experimental autoimmune myocarditis. , 2013, Biochimica et biophysica acta.

[6]  C. Weber,et al.  Neutrophil-Derived Cathelicidin Promotes Adhesion of Classical Monocytes , 2013, Circulation research.

[7]  Teruaki Wajima,et al.  Neutrophil TRPM2 channels are implicated in the exacerbation of myocardial ischaemia/reperfusion injury. , 2013, Cardiovascular research.

[8]  A. Mildner,et al.  Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis. , 2013, Immunity.

[9]  J. Fallowfield,et al.  Edinburgh Research Explorer Differential Ly-6C expression identifies the recruited macrophage phenotype, which orchestrates the regression of murine liver fibrosis Differential Ly-6C expression identi fi es the recruited macrophage phenotype, which orchestrates the regression of murine liver fi brosis , 2022 .

[10]  Huaxi Xu,et al.  IL-17 contributes to cardiac fibrosis following experimental autoimmune myocarditis by a PKCβ/Erk1/2/NF-κB-dependent signaling pathway. , 2012, International immunology.

[11]  N. Rose,et al.  Macrophage diversity in cardiac inflammation: a review. , 2012, Immunobiology.

[12]  N. Frangogiannis.  Matricellular proteins in cardiac adaptation and disease. , 2012, Physiological reviews.

[13]  Sandeep Sagar,et al.  Myocarditis , 2012, The Lancet.

[14]  Alberto Mantovani,et al.  Macrophage plasticity and polarization: in vivo veritas. , 2012, The Journal of clinical investigation.

[15]  Jing Yuan,et al.  Interleukin-17A contributes to myocardial ischemia/reperfusion injury by regulating cardiomyocyte apoptosis and neutrophil infiltration. , 2012, Journal of the American College of Cardiology.

[16]  E. Pamer,et al.  Monocyte recruitment during infection and inflammation , 2011, Nature Reviews Immunology.

[17]  H. Fujii,et al.  Role of IL-17A in Neutrophil Recruitment and Hepatic Injury after Warm Ischemia–Reperfusion Mice , 2011, The Journal of Immunology.

[18]  M. Merad,et al.  Dendritic cell and macrophage heterogeneity in vivo. , 2011, Immunity.

[19]  Yvonne Bordon.  T cell responses: CD4s work the doors , 2011, Nature reviews. Immunology.

[20]  Maria Papatriantafyllou.  Cytokines: GM-CSF in focus , 2011, Nature Reviews Immunology.

[21]  Y. Iwakura,et al.  Interleukin-17A Is Dispensable for Myocarditis but Essential for the Progression to Dilated Cardiomyopathy , 2010, Circulation research.

[22]  T. Wynn,et al.  Bleomycin and IL-1β–mediated pulmonary fibrosis is IL-17A dependent , 2010, The Journal of experimental medicine.

[23]  Y. Liao,et al.  Th17 Cells Facilitate the Humoral Immune Response in Patients with Acute Viral Myocarditis , 2010, Journal of Clinical Immunology.

[24]  M. Kodama,et al.  Lipocalin-2/neutrophil gelatinase-B associated lipocalin is strongly induced in hearts of rats with autoimmune myocarditis and in human myocarditis. , 2010, Circulation journal : official journal of the Japanese Circulation Society.

[25]  J. Towbin,et al.  Frequency of cardiac death in children with idiopathic dilated cardiomyopathy. , 2009, The American journal of cardiology.

[26]  P. Libby,et al.  Identification of Splenic Reservoir Monocytes and Their Deployment to Inflammatory Sites , 2009, Science.

[27]  S. Gaffen.  Structure and signalling in the IL-17 receptor family , 2009, Nature Reviews Immunology.

[28]  Thomas Korn,et al.  IL-17 and Th17 Cells. , 2009, Annual review of immunology.

[29]  K. Tsuneyama,et al.  Hepatic IL-17 responses in human and murine primary biliary cirrhosis. , 2009, Journal of autoimmunity.

[30]  D. Pennell,et al.  The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. , 2008, European heart journal.

[31]  S. Gaffen,et al.  The Interleukin-17 Receptor Plays a Gender-Dependent Role in Host Protection against Porphyromonas gingivalis-Induced Periodontal Bone Loss , 2008, Infection and Immunity.

[32]  M. Kimura,et al.  Interleukin-13 protects against experimental autoimmune myocarditis by regulating macrophage differentiation. , 2008, The American journal of pathology.

[33]  P. Libby,et al.  The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions , 2007, The Journal of experimental medicine.

[34]  S. Gordon,et al.  Monocyte and macrophage heterogeneity , 2005, Nature Reviews Immunology.

[35]  S. Windecker,et al.  Safety and efficacy of subcutaneous-only granulocyte-macrophage colony-stimulating factor for collateral growth promotion in patients with coronary artery disease. , 2005, Journal of the American College of Cardiology.

[36]  S. Ogawa,et al.  Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction. , 2004, Journal of the American College of Cardiology.

[37]  J. Vinten-johansen.  Involvement of neutrophils in the pathogenesis of lethal myocardial reperfusion injury. , 2004, Cardiovascular research.

[38]  Sarah L. Gaffen,et al.  Functional Cooperation between Interleukin-17 and Tumor Necrosis Factor-α Is Mediated by CCAAT/Enhancer-binding Protein Family Members* , 2004, Journal of Biological Chemistry.

[39]  Steffen Jung,et al.  Blood monocytes consist of two principal subsets with distinct migratory properties. , 2003, Immunity.

[40]  Thomas D. Schmittgen,et al.  Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.

[41]  T. K. van den Berg,et al.  Apoptosis of macrophages induced by liposome-mediated intracellular delivery of clodronate and propamidine. , 1996, Journal of immunological methods.

[42]  P. Allen,et al.  The role of T cells in myosin-induced autoimmune myocarditis. , 1993, Clinical immunology and immunopathology.

[43]  J. Deckers,et al.  Demographic features and prevalence of idiopathic myocarditis in patients undergoing endomyocardial biopsy. , 1993, The American journal of cardiology.

[44]  P. Allen,et al.  Myosin-induced acute myocarditis is a T cell-mediated disease. , 1991, Journal of immunology.

[45]  P. Libby,et al.  Chigh Monocytes Depend on Nr 4 a 1 to Balance Both Inflammatory and Reparative Phases in the Infarcted Myocardium , 2014 .

[46]  Early Predictors of Survival to and After Heart Transplantation in Children With Dilated Cardiomyopathy , 2013 .

[47]  N. Rose,et al.  Pathogenesis of myocarditis and dilated cardiomyopathy. , 2008, Advances in immunology.

[48]  Rajni B. Sharma,et al.  Animal models for autoimmune myocarditis and autoimmune thyroiditis. , 2004, Methods in molecular medicine.

[49]  W. Edwards,et al.  Myocarditis. A histopathologic definition and classification. , 1987, The American journal of cardiovascular pathology.

[50]  Thomas D. Schmittgen,et al.  Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2 2 DD C T Method , 2022 .

[51]  P. Libby,et al.  Integrative Ly-6C high Monocytes Depend on Nr4a1 to Balance Both Inflammatory and Reparative Phases in the Infarcted Myocardium , 2022 .