Anti-CD177 (full length) polyclonal antibody

Background: 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. Objective: 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). Methods: 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. Results: 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. Conclusion: 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. (C) 2016 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.