Fine-tuning levels of filamins a and b as a specific mechanism sustaining Th2 lymphocyte functions

Kilian Maire, Léa Chamy, Samira Ghazali, Manon Carratala-Lasserre, Margot Zahm, Clément Bouisset, Arnaud Métais, Lucie Combes-Soia, Lidia Fuente-Vizuete, Hussein Trad, Adeline Chaubet, Magali Savignac, Anne Gonzalez de Peredo, Arun Subramaniam, Olivier Joffre, Pierre G. Lutz () and Isabelle Lamsoul ()
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Kilian Maire: University of Toulouse, CNRS, Inserm, UPS
Léa Chamy: University of Toulouse, CNRS, Inserm, UPS
Samira Ghazali: University of Toulouse, CNRS, Inserm, UPS
Manon Carratala-Lasserre: University of Toulouse, CNRS, Inserm, UPS
Margot Zahm: University of Toulouse, CNRS, Inserm, UPS
Clément Bouisset: University of Toulouse, CNRS, Inserm, UPS
Arnaud Métais: Institut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, UPS
Lucie Combes-Soia: Institut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, UPS
Lidia Fuente-Vizuete: University of Toulouse, CNRS, Inserm, UPS
Hussein Trad: University of Toulouse, CNRS, Inserm, UPS
Adeline Chaubet: University of Toulouse, CNRS, Inserm, UPS
Magali Savignac: University of Toulouse, CNRS, Inserm, UPS
Anne Gonzalez de Peredo: Institut de Pharmacologie et de Biologie Structurale (IPBS), Université de Toulouse, CNRS, UPS
Arun Subramaniam: Sanofi Immunology and Inflammation Research Therapeutic Area
Olivier Joffre: University of Toulouse, CNRS, Inserm, UPS
Pierre G. Lutz: University of Toulouse, CNRS, Inserm, UPS
Isabelle Lamsoul: University of Toulouse, CNRS, Inserm, UPS

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Augmenting the portfolio of therapeutics for type 2-driven diseases is crucial to address unmet clinical needs and to design personalized treatment schemes. An attractive therapy for such diseases would consist in targeting the recruitment of T helper 2 (Th2) lymphocytes to inflammatory sites. Herein, we show the degradation of filamins (FLN) a and b by the ASB2α E3 ubiquitin ligase as a mechanism sustaining Th2 lymphocyte functions. Low levels of FLNa and FLNb confer an elongated shape to Th2 lymphocytes associated with efficient αVβ3 integrin-dependent cell migration. Genes encoding the αVβ3 integrin and ASB2α belong to the core of Th2-specific genes. Using genetically modified mice, we find that increasing the levels of FLNa and FLNb in Th2 lymphocytes reduces airway inflammation through diminished Th2 lymphocyte recruitment in inflamed lungs. Collectively, our results highlight ASB2α and its substrates FLNa and FLNb to alter Th2 lymphocyte-mediated responses.

Date: 2024
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DOI: 10.1038/s41467-024-53768-3

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