{"database":"bioimages","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":[null],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-BIAD1497"],"repository":["bioimages"],"figure_sub":["Specimen","Study Component","organisation","Biosample","Associations","Image acquisition"],"pubmed_authors":["Melina Messing"],"additional_accession":[]},"is_claimable":false,"name":"Type-2 innate signals are dispensable for skeletal muscle regeneration and pathology linked to Duchenne muscular dystrophy","description":"Immune responses play an integral role in skeletal muscle regeneration. In the genetically inherited muscle disease Duchenne muscular dystrophy (DMD), muscle regeneration is disrupted, leading to chronic inflammation, fibrosis, and early mortality. Previously, it has been suggested that type-2 innate immune cells, particularly eosinophils and their production of IL-4, play an essential role in effective muscle regeneration after acute injury. We here re-investigate the role of eosinophils in skeletal muscle repair using mice deficient in eosinophils (ΔdblGATA), or deficient in IL-4R/IL-13R signaling through STAT6 (Stat6-/-). We show that neither deficiency has an impact on skeletal muscle regeneration in response to acute injury as quantified by fiber size, immune cell infiltration, or mus","dates":{"release":"2024-11-30T00:00:00Z","modification":"2025-01-21T04:04:15.436Z","creation":"2024-11-30T23:57:55.465Z"},"accession":"S-BIAD1497","cross_references":{}}