Hier finden Sie wissenschaftliche Publikationen aus den Fraunhofer-Instituten.

Phenotypic characterization of blood and lung ILC2 in asthmatics undergoing segmental allergen provocation

: Pardali, Katerina; Winkler, Carla; Hochdorfer, T.; Cavallin, A.; Hasselberg, A.; Vaarala, O.; Müller, Meike; Lüer, Katrin


American Journal of Respiratory and Critical Care Medicine 197 (2018), Art. A5966
ISSN: 1073-449X
ISSN: 0003-0805
ISSN: 1535-4970
American Thoracic Society (ATS International Conference) <2018, San Diego/Calif.>
Fraunhofer ITEM ()

Aims and objective: To characterise the phenotype and function of human ILC2 in acute allergic lung inflammation. Methods: We isolated human ILC2 from blood and bronchoalveolar lavage (BAL) of asthmatic patients (n=7) before and 24h after a segmental allergen challenge with either grass or house dust mite allergen). Cells were characterized by surface marker expression, cytokine secretion and transcriptomics analysis. Mediators in BAL, serum and cell culture supernatants were measured by multiplex ELISA. Results: Segmental allergen challenge induced a Th2 inflammation characterised by BAL eosinophils increasing from 0.9±0.5% to 75±14.4% and accompanied by an increase in Th2 cytokines. While numbers of ILC2 in blood decreased upon allergen challenge (6.3 fold; p=0.047) a 25 fold increase was observed in the BAL from allergen challenged lung segments (p=0.016). BAL ILC2 showed lower expression of CCR4 than blood ILC2. The ligands for CCR4; CCL17 and CCL22 were increased in BAL after allergen provocation (p<0.05). BAL ILC2 revealed a distinct mRNA expression profile indicating up-regulation of the cytokine production, costimulatory and antigen presenting functions. ILC2 derived from BAL after challenge secreted spontaneously IL-5 and IL-13 in contrast to blood ILC2. Conclusion: During an acute allergic airway inflammation the blood ILC2 infiltrate the lung and acquire an activated phenotype with markers indicating a role in local T-cell activation. while blood ILC2 t do not change their phenotype in response to the inflammation in lung.