We are proposing to target Innate Lymphoid Cells 2 (ILC2s), a subset that has been frequently implicated in inflammatory diseases, such as severe asthma. ILC2s are major players in allergic asthma and are abundantly present as tissue resident cells in the lung, both in human and mouse. Strikingly, the induction of allergic asthma in a mouse model deficient in ILC2s is abolished. In addition, the transfer of ILC2s back in the same mouse recapitulates the pathology. Mechanistically, activated ILC2s are the main producer of type 2 cytokines that sustain the chronicity of asthma by recruiting other inflammatory and pathogenic cells, notably eosinophils, and finally drive hyperresponsiveness and mucous hypersecretion. In humans, ILC2s are increased in the peripheral blood mononuclear cells (PBMCs) of patients with allergic asthma compared to healthy controls. They are also found in sputum and PBMCs of patients with severe, eosinophilic asthma compared to mild forms of asthma. Collectively, these data highlight the significance of ILC2s in allergic inflammation and emphasize the idea to target those cells for therapeutic purposes. MInfla-Tilc is a translational and integrated project aiming to launch an innovative therapeutic monoclonal antibody (mAb) treatment against ILC2s to control severe asthma.
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Funding SchemeERC-POC-LS - ERC Proof of Concept Lump Sum Pilot