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Gastvortrag Jörg Fritz: Lymphoide Zellen


19. Dezember 2022
11:00 - 12:00

Emanuel Merck Auditorium
Institut für Medizinische Genetik
Währinger Straße 10

Der Sonderforschungsbereich F83 „Metabolische Regulierung der Gewebeintegrität“ des FWF lädt am Montag, 19. Dezember 2022, zu einem internationalen Gastvortrag. Jörg Fritz vom McGill Research Center on Complex Traits (MRCCT) der McGill University in Montreal hält einen Vortrag zum Thema "Regulation of Group 2 Innate Lymphoid Cells (ILC2s)". Das Seminar findet im Emanuel Merck Auditorium am Institut für Medizinische Genetik (Währinger Straße 10) statt. Beginn: 11 Uhr.

Monday, December 19th  2022: 11 am
SFB F83 Immunometabolism Seminar
Jörg FRITZ, PhD (Director, McGill Research Center on Complex Traits (MRCCT), McGill University, Montreal, Quebec, Canada)
"Regulation of Group 2 Innate Lymphoid Cells (ILC2s)"
Where: Institute of Medical Genetics, Emanuel Merck Auditorium, 1st Floor, Währinger Straße 10, 1090 Vienna.

Abstract: Group 2 innate lymphoid cells (ILC2s) comprise a remarkably potent source of cytokines and have been shown to be central in instructing and sustaining human type 2 immunopathologies including allergic lung inflammation and asthma. ILC2s directly sense alarmins such as interleukin (IL)-33 following allergen or microbial challenge, driving ILC2 proliferation and type 2 cytokine production. However, the precise molecular signatures of IL-33-mediated ILC2 activation remain unknown. Using an RNA-sequencing approach we revealed that IL-33 stimulation rapidly induces the expression of diacylglycerol acyltransferase 2 (DGAT2), an enzyme known catalyze triacylglycerol synthesis and lipid storage in lipid droplets. In addition, we observed that IL-33-mediated ILC2 activation leads to elevated fatty acid uptake and storage that requires activity of fatty acid binding protein 5 (FABP5) and fatty acid transporter protein 2 (FATP2). Importantly, lipidomic analysis revealed a selective role of DGAT2 in fatty acid metabolism in ILC2. Moreover, in a preclinical mouse model of allergic airway inflammation, we demonstrate that DGAT2 inhibition decreases ILC2 proliferation, lung inflammation and airway hyperreactivity. These observations highlight the crucial role of DGAT2 in ILC2 biology and ILC2-mediated lung inflammation and suggest that DGAT2 inhibitors should be considered for the treatment of type 2 immunopathologies.