title: Immune Mechanisms in Pulmonary Fibrosis.
abstract: Pulmonary fibrosis, particularly idiopathic pulmonary fibrosis, represents a chronic and progressive disease with high mortality and limited therapeutic options. Excessive deposition of extracellular matrix proteins results in fibrotic remodeling, alveolar destruction, and irreversible loss of lung function. Both innate and adaptive immune mechanisms contribute to fibrogenesis at several cellular and noncellular levels. Here, we summarize and discuss the role of immune cells (T cells, neutrophils, macrophages, and fibrocytes) and soluble mediators (cytokines and chemokines) involved in pulmonary fibrosis, pointing toward novel immune-based therapeutic strategies in the field.
authors.affiliation: 1 Pediatric Infectiology, Immunology, and Cystic Fibrosis, Children's Hospital of the University of Tübingen, Tübingen, Germany.
authors.forename: Saeed
authors.initials: S
authors.lastname: Kolahian
authors.affiliation: 2 Comprehensive Pneumology Center, Institute of Lung Biology and Disease, University Hospital, Ludwig Maximilians University and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany; and.
authors.forename: Isis E
authors.initials: IE
authors.lastname: Fernandez
authors.affiliation: 2 Comprehensive Pneumology Center, Institute of Lung Biology and Disease, University Hospital, Ludwig Maximilians University and Helmholtz Zentrum München, Member of the German Center for Lung Research, Munich, Germany; and.
authors.forename: Oliver
authors.initials: O
authors.lastname: Eickelberg
authors.affiliation: 1 Pediatric Infectiology, Immunology, and Cystic Fibrosis, Children's Hospital of the University of Tübingen, Tübingen, Germany.|3 Immunology, Inflammation, and Infectious Diseases Discovery and Translational Area, Roche Pharma Research and Early Development, Roche Innovation Center Basel, Basel, Switzerland.
authors.forename: Dominik
authors.initials: D
authors.lastname: Hartl
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007962:Leukocytes / Q000276:immunology; D008954:Models, Biological; D011658:Pulmonary Fibrosis / Q000276:immunology* / Q000628:therapy
chemical_list: D016207:Cytokines
keywords: T cells; fibrosis; immunity; lung; neutrophils