title: Leptin Enhances TH2 and ILC2 Responses in Allergic Airway Disease.
abstract: Allergic asthma and obesity are the leading health problems in the world. Many studies have shown that obesity is a risk factor of development of asthma. However, the underlying mechanism has not been well established. In this study, we demonstrate that leptin, an adipokine elevated in obese individuals, promoted proliferation and survival of pro-allergic type 2 helper T cells and group 2 innate lymphoid cells and production of type 2 cytokines, which together contribute to allergic responses. Leptin activates mTORC1, MAPK, and STAT3 pathways in TH2 cells. The effects of leptin on TH2 cell proliferation, survival, and cytokine production are dependent on the mTORC1 and MAPK pathways as revealed by specific inhibitors. In vivo, leptin-deficiency led to attenuated experimental allergic airway inflammation. Our results thus support that obesity-associated elevation of leptin contributes to the increased susceptibility of asthma via modulation of pro-allergic lymphocyte responses.
authors: From the Departments of Molecular Genetics and Microbiology, Pathology, and.
authors: Handong
authors: H
authors: Zheng
authors: From the Departments of Molecular Genetics and Microbiology, Pathology, and Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131, and.
authors: Xing
authors: X
authors: Zhang
authors: From the Departments of Molecular Genetics and Microbiology, Pathology, and.
authors: Eliseo F
authors: EF
authors: Castillo
authors: Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131, and Department of Metabolism and Endocrinology, Metabolic Syndrome Research Center, The Second Xiangya Hospital, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, National Clinical Research Center for Metabolic Diseases, Changsha, Hunan 410011, China.
authors: Yan
authors: Y
authors: Luo
authors: Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131, and meilianliu@salud.unm.edu.
authors: Meilian
authors: M
authors: Liu
authors: From the Departments of Molecular Genetics and Microbiology, Pathology, and xyang@salud.unm.edu.
authors: Xuexian O
authors: XO
authors: Yang
mesh_terms: D000818:Animals; D001249:Asthma / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D049109:Cell Proliferation; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000276:immunology; D020738:Leptin / Q000235:genetics / Q000276:immunology*; D020935:MAP Kinase Signaling System / Q000235:genetics / Q000276:immunology*; D000076222:Mechanistic Target of Rapamycin Complex 1; D051379:Mice; D018345:Mice, Knockout; D046912:Multiprotein Complexes / Q000235:genetics / Q000276:immunology; D009765:Obesity / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000276:immunology; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology* / Q000473:pathology
chemical_list: D016207:Cytokines; D020738:Leptin; D046912:Multiprotein Complexes; D050796:STAT3 Transcription Factor; D000076222:Mechanistic Target of Rapamycin Complex 1; D058570:TOR Serine-Threonine Kinases; D048049:Extracellular Signal-Regulated MAP Kinases
keywords: T helper cells; asthma; inflammation; innate immunity; leptin