Coordination

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Microbial and non-infectious insults trigger distinct inflammatory response patterns that fundamentally differ, dependent on the stimulus and the affected tissue. The choice of the right quality of immune response determines whether it will be efficient and beneficial or, on the contrary, cause additional damage. Type 2 immunity designates the response pattern activated by helminth infection, allergens and venoms, but also during the repair process in wounded tissue. It is defined by a dominant milieu of the cytokines IL-4, IL-5 and IL- 13. The term “type 2 response” embraces both the ‘innate’ type 2 responses of tissues and the subsequent adaptive TH2 and IgE responses, the latter being instructed by the initial innate response. While type 2 immunity serves key functions in defense, tissue repair and metabolic regulation, and is the driver of allergic and fibrotic disease, factors controlling type 2 responses are still unclear. We aim to elucidate the fundamental mechanisms that induce and regulate type 2 immunity in normal tissues, and in pathologies where type 2 immunity is required for protection, or is a promoter of disease. FOR2599 integrates leading experts in the biology of important cell types that contribute to type 2 responses, including M2 macrophages, innate lymphoid cells, dendritic cells, eosinophilic and basophilic granulocytes and mast cells. The group combines expertise in key signaling pathways regulating type 2 responses and has available a unique spectrum of innovative genetic mouse lines and in vivo disease models. This enables tremendous synergy, putting FOR2599 in an ideal position to elucidate how the various tissue cells interact to mount and regulate a local type 2 response in steady state or under conditions of tissue stress of different nature and intensity.