PT  - JOURNAL ARTICLE
AU  - Jirmo, Adan Chari
AU  - Deluca, David S.
AU  - Grychtol, Ruth
AU  - Dittrich- Breiholz, Oliver
AU  - Happle, Christine
AU  - Hansen, Gesine
TI  - Influence of IL-17 on transcriptional profiles of lung and peribronchial lymph nodes dendritic cells in steady and antigen exposed conditions
AID  - 10.1183/13993003.congress-2019.PA5215
DP  - 2019 Sep 28
TA  - European Respiratory Journal
PG  - PA5215
VI  - 54
IP  - suppl 63
4099  - http://erj.ersjournals.com/content/54/suppl_63/PA5215.short
4100  - http://erj.ersjournals.com/content/54/suppl_63/PA5215.full
SO  - Eur Respir J2019 Sep 28; 54
AB  - Background: Increased Interleukin 17 (IL-17) levels are observed in inflammatory diseases such as allergic asthma, psoriasis, and rheumatoid arthritis. Nevertheless, with the exception of its role in attracting neutrophils to inflammatory sites, how IL-17 influences other leukocytes is yet to be fully elucidated.Objective: Our aim in this study is to understanding how IL-17 influences transcriptomic patterns of conventional pulmonary dendritic cells both in steady and antigen exposed conditionsMethods: We made a comprehensive comparative transcriptomic analysis of lungs and lung draining lymph nodes derived conventional dendritic cells from wild type as well as IL-17A/F double knockout mice in an experimental model of allergic asthma.Results: We used previously described gene sets in order to carry out a comprehensive comparative analysis between IL-17 sufficient versus IL-17 deficient cDCs transcriptomes. We hereby show that, absence of IL-17 affects various transcriptional programs associated with the ability of DCs to migrate, present antigen as well as co-stimulation of effector cells. We have used bioinformatics tools in order to illustrate affected migration, antigen presentation and co-stimulation pathways.Conclusions: Our transcriptomic analysis shows that IL-17 enhances migratory as well as antigen presenting potential of cDCs. We thus conclude that functional potential of DC could be impaired through targeting IL-17 in order to control inflammation.FootnotesCite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA5215.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).