Human group 2 innate lymphoid cells do not express the IL-5 receptor

Christopher E Brightling,Batika M.J Rana,Adam K.A Wright,David J Cousins,Cathryn Weston

doi:10.1016/j.jaci.2017.04.025

Abstract

This work was part funded by (for CEB) Airway Disease Predicting Outcomes through Patient Specific Computational Modelling (AirPROM) project (funded through FP7 EU grant), Wellcome Senior Fellowship, (for DJC) Medical Research Council (MRC) and Asthma UK (Centre Grant: G1000758), from the NIHR Biomedical Research Centre based at Guy's and St Thomas' NHS Foundation Trust and King's College London, an equipment grant from the Midlands Asthma and Allergy Research Association (MAARA) and (for CEB and DJC) the National Institute for Health Research (NIHR) Leicester Respiratory Biomedical Unit. BMJR was funded by an MRC and Asthma UK PhD studentship. This paper presents independent research funded by the NIHR.

Highlights

To the Editor: Eosinophils, cardinal effector cells of type 2 inflammation, contribute to the clinical and immunopathologic manifestations of asthma[1] and chronic obstructive pulmonary disease[2] inflammatory endotypes
Eosinophil biology is governed by IL-5, a cytokine that binds with high affinity to a specific IL-5 receptor a subunit (IL-5Ra) before forming a heterodimeric receptor complex with the b subunit.[3]
Because the IL-5-IL-5R axis appears to be restricted to eosinophils and basophils,[6] therapeutic regulation of these cells through the neutralization of circulating IL-51 or IL5Ra ligation,[1,2] have emerged as effective strategies to deplete blood, tissue, and airway eosinophils and reduce exacerbation rates and improve lung function.[1]

Summary

Letters to the Editor

To the Editor: Eosinophils, cardinal effector cells of type 2 inflammation, contribute to the clinical and immunopathologic manifestations of asthma[1] and chronic obstructive pulmonary disease[2] inflammatory endotypes. Data from these 7 subjects consistently show that tissuederived basophils express the IL-5Ra whereas tissue-derived ILC2s do not (Fig 2, H). It would be desirable to extend our blood and tissue observations to investigate whether ILC2s in bronchial biopsies from patients with asthma express IL-5Ra, the paucity of tissue ILCs and the need for multiple immunological markers to positively identify them severely limits this approach These results extend the list of cells[6] that are known not to express the IL5Ra subunit, specific for the biological activities of IL-5. The rest of the authors declare that they have no relevant conflicts of interest

METHODS

Flow cytometry

Findings

Control n