title: IL-17RB+granulocytes are associated with airflow obstruction in asthma.
abstract: Interleukin (IL)-25 (IL-17E) is a proinflammatory cytokine that plays an important role in the T-helper type 2 cell pathway. The effects of IL-25 are mediated by its specific receptor, IL-17RB. Previous studies have defined an IL-17RB+granulocyte population known as type 2 myeloid (T2M) cells that express T-helper type 2 cell cytokines. The correlation of IL-17RB+granulocytes, T2M cells, and asthma parameters is unknown.
  
  
  
  To investigate the relation of IL-17RB+granulocytes (and its subset, T2M cells) in patients with asthma with clinical parameters including spirometric values and the Asthma Control Test (ACT).
  
  
  
  Peripheral blood from subjects with asthma and healthy controls was collected and analyzed by flow cytometry. Granulocytes were gated for IL-17RB+, T2M (CD11b+CD16+CD177+IL-17RB+), and eosinophil (CD16-) populations. Spirometry testing was performed on subjects with asthma. ACT scores and medical histories were collected by questionnaire and chart review. Correlations of IL-17RB+cells and T2M cells with spirometry and ACT score were analyzed.
  
  
  
  Percentages of IL-17RB+granulocytes and T2M cells were larger in subjects with asthma than in controls. Furthermore, percentages of the 2 cell populations were negatively correlated with degree of airway obstruction as measured by the ratio of percentage-predicted forced expiratory volume in 1 second to force vital capacity (r = -0.17, P = .043 for IL-17RB+granulocytes; r = -0.32, P = .03 for T2M cells). There was no correlation with ACT score. The percentage of eosinophils was increased in subjects with asthma. However, IL-17RB+eosinophil percentages were similar between subjects with asthma and controls and did not correlate with any clinical parameter.
  
  
  
  IL-17RB+granulocytes and T2M cells from peripheral blood were increased in subjects with asthma, and the 2 cell types correlated with degree of airflow obstruction.
authors.affiliation: Division of Allergy and Immunology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan.
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
authors.forename: Nicholas W
authors.initials: NW
authors.lastname: Lukacs
authors.affiliation: Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
authors.forename: Matthew A
authors.initials: MA
authors.lastname: Schaller
authors.affiliation: Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
authors.forename: Bryan
authors.initials: B
authors.lastname: Petersen
authors.affiliation: Division of Allergy and Immunology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan. Electronic address: abaptist@med.umich.edu.
authors.forename: Alan P
authors.initials: AP
authors.lastname: Baptist
mesh_terms: D000328:Adult; D000402:Airway Obstruction / Q000276:immunology / Q000378:metabolism* / Q000473:pathology*; D001249:Asthma / Q000276:immunology / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D015415:Biomarkers; D016022:Case-Control Studies; D004804:Eosinophils; D005260:Female; D005455:Fluorescent Antibody Technique; D005541:Forced Expiratory Volume; D006098:Granulocytes / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D016130:Immunophenotyping; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D018123:Receptors, Interleukin / Q000378:metabolism*; D053722:Receptors, Interleukin-17; D012129:Respiratory Function Tests
chemical_list: D015415:Biomarkers; C408922:IL17RB protein, human; D018123:Receptors, Interleukin; D053722:Receptors, Interleukin-17