Extract
In recent 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 asthma patients. To investigate this, we focused on the Th2-stimulatory molecules (CD86, OX40L) and Th2-inhibitory molecule PD-L1 [6–8].
Abstract
Proportions of conventional dendritic cell subsets and the expression of co-stimulatory and co-inhibitory molecules in cDC2s are altered in asthma patients. These changes are most pronounced in asthmatics with frequent exacerbations. http://bit.ly/2wbb8UJ
Acknowledgements
We would like to thank all the participants of the study, and the physicians and research nurses of the Franciscus Gasthuis (Rotterdam, the Netherlands) for their assistance in study design and inclusion of participants. Additionally, we would like to thank B.W.S. Li, E. van der Ploeg, and M.J.W. de Bruijn for their assistance during the project.
Footnotes
Conflict of interest: H. Vroman reports grants from EAACI Young Investigator's Grant, during the conduct of the study.
Conflict of interest: I. Tindemans has nothing to disclose.
Conflict of interest: M. Lukkes has nothing to disclose.
Conflict of interest: M. van Nimwegen has nothing to disclose.
Conflict of interest: G.M. de Boer has nothing to disclose.
Conflict of interest: G.A. Tramper-Stranders reports grants from OM Pharma, ESPID and Stichting Coolsingel, during the conduct of the study, which were all paid directly to a research foundation.
Conflict of interest: G-J. Braunstahl reports grants from GSK, Novartis, AstraZeneca, Chiesi and Sanofi, outside the submitted work.
Conflict of interest: R.W. Hendriks reports grants from Netherlands Lung Foundation, outside the submitted work.
Conflict of interest: M. Kool reports grants from Netherlands Lung Foundation, during the conduct of the study.
Support statement: This study was partly supported by a long-term EAACI research fellowship to H. Vroman and a Junior investigator Grant from the Netherlands Lung Foundation (4.2.13.054JO) to M. Kool. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received April 26, 2019.
- Accepted February 4, 2020.
- Copyright ©ERS 2020