title: Enhanced innate type 2 immune response in peripheral blood from patients with asthma.
abstract: BACKGROUND
  In mice, group 2 innate lymphoid cells (ILC2s) likely mediate helminth immunity, inflammation, and tissue repair and remodeling. However, the involvement of ILC2s in human diseases, such as asthma, is not well understood.
  
  
  OBJECTIVE
  The goals of this study were to investigate whether peripheral blood specimens can be used to monitor innate type 2 immunity in human subjects and to examine whether ILC2s are involved in human asthma.
  
  
  METHODS
  PBMCs from subjects with allergic asthma (AA), subjects with allergic rhinitis (AR), or healthy control (HC) subjects were cultured in vitro with IL-25 or IL-33. Flow cytometry and cell sorting were used to identify, isolate, and quantitate ILC2s in PBMCs.
  
  
  RESULTS
  Human PBMCs produced IL-5 and IL-13 when stimulated with IL-33 or IL-25 in the presence of IL-2 without antigens. In addition, IL-7 or thymic stromal lymphopoietin were able to replace IL-2. The cell population with phenotypic ILC2 characteristics, lineage(-)CD127(+)CRTH2(+) cells, responded to IL-33 and produced large quantities of IL-5 and IL-13 but undetectable levels of IL-4. PBMCs from subjects with AA produced significantly larger amounts of IL-5 and IL-13 in response to IL-25 or IL-33 than from subjects with AR or HC. The prevalence of ILC2s in blood was greater in the AA group than in the AR group or the HC group.
  
  
  CONCLUSIONS
  Innate type 2 immune responses are increased in asthma but not in AR, suggesting potential differences in the immunopathogenesis of these diseases. Peripheral blood is useful for evaluating innate type 2 immunity in humans.
authors.affiliation: Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, Minn; Department of Immunology, Mayo Clinic, Rochester, Minn.
authors.forename: Kathleen R
authors.initials: KR
authors.lastname: Bartemes
authors.affiliation: Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, Minn.
authors.forename: Gail M
authors.initials: GM
authors.lastname: Kephart
authors.affiliation: Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, Minn.
authors.forename: Stephanie J
authors.initials: SJ
authors.lastname: Fox
authors.affiliation: Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, Minn; Department of Immunology, Mayo Clinic, Rochester, Minn. Electronic address: kita.hirohito@mayo.edu.
authors.forename: Hirohito
authors.initials: H
authors.lastname: Kita
mesh_terms: D001249:Asthma / Q000175:diagnosis / Q000276:immunology*; D001775:Blood Circulation; D002454:Cell Differentiation; D002469:Cell Separation; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007113:Immunity, Innate; D053699:Interleukin-7 Receptor alpha Subunit / Q000378:metabolism; D007378:Interleukins / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D011971:Receptors, Immunologic / Q000378:metabolism; D011982:Receptors, Prostaglandin / Q000378:metabolism; D065631:Rhinitis, Allergic / Q000175:diagnosis / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology
chemical_list: D053699:Interleukin-7 Receptor alpha Subunit; D007378:Interleukins; D011971:Receptors, Immunologic; D011982:Receptors, Prostaglandin; C036293:prostaglandin D2 receptor
keywords: IL-13; IL-25; IL-33; IL-5; ILC2; allergy; asthma; innate immunity