Type II conventional DCs of asthmatic patients with frequent exacerbations have an altered phenotype and frequency.

In the last decades it has become clear that dendritic cells (DCs) critically contribute to the development of T helper 2 (Th2)-mediated allergic diseases, such as asthma. Two main conventional DC (cDC) subsets, type 1 cDCs (cDC1s) and cDC2s, can be identified based on the expression of cell-surface molecules and transcription factors [1]. Using mouse models in which specific DC subsets are targeted or by adoptive transfer of DC subsets, it has been shown that upon activation in the airways cDC2s migrate towards the lung-draining lymph node where they induce allergen-specific Th2 cells, which subsequently promote eosinophilic airway inflammation [2]. The role of cDC1s in asthma is more controversial, although most recent reports indicate that cDC1s can efficiently suppress allergic airway inflammation [3], either by the induction of regulatory T cells [4] or through increased interleukin (IL)-12 production [5]. These functional properties of DC subsets were evaluated in mouse models, but to date it is unclear how these findings reflect the characteristics of cDC subsets in asthmatic patients with different disease severities. Therefore, we questioned whether DC subset frequencies and the surface expression of co-stimulatory and co-inhibitory molecules differ between healthy persons and asthmatic patients. To investigate this, we focused on the Th2-stimulatory molecules (CD86, OX40L) and Th2-inhibitory molecule PD-L1 [6–8]. Footnotes This manuscript has recently been accepted for publication in the European Respiratory Journal . It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article. Conflict of interest: Dr. Vroman reports grants from EAACI Young Investigatoru0027s Grant, during the conduct of the study. Conflict of interest: Dr. Tindemans has nothing to disclose. Conflict of interest: Dr. Lukkes has nothing to disclose. Conflict of interest: Dr. van Nimwegen has nothing to disclose. Conflict of interest: Dr. de Boer has nothing to disclose. Conflict of interest: Dr. Tramper reports grants from OM Pharma, grants from ESPID, grants from Stichting Coolsingel, during the conduct of the study; which were all paid directly to a research foundation Conflict of interest: Dr. Braunstahl reports grants from GSK, grants from Novartis, grants from AstraZeneca, grants from Chiesi, grants from Sanofi, outside the submitted work. Conflict of interest: Dr. Hendriks reports grants from Netherlands Lung Foundation, outside the submitted work. Conflict of interest: Dr. Kool reports grants from Netherlands Lung Foundation, during the conduct of the study.