{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301384/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by array"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301384"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Nanostring gene expression profiling in a mouse model of antibody-mediated rejection of kidney allografts","description":"Acute and chronic antibody mediated rejection (ABMR) continues to decrease clinical kidney graft function and survival. Dysregulated donor-specific antibody (DSA) responses are induced in B6.CCR5-/- recipients of complete MHC-mismatched A/J kidney allografts with NK cells playing a critical role in the acute ABMR. We tested the role of neutrophils in ABMR by transplanting A/J kidneys to CCR5-/- mice with a deletion in the neutrophil serine protease cathepsin G. Whereas B6.CCR5-/- recipients rejected all kidney allografts between days 18-25, 70% of allografts survived beyond day 60 in B6.CCR5-/-cG-/- recipients. At days 15-17 post-transplant DSA titers in B6.CCR5-/-cG-/- recipients were 24.3-fold higher than those in wild-type C57BL/6 allograft recipients. Allografts from B6.CCR5-/-cG-/- recipients on days 45 and 60 had typical characteristics of chronic graft injury including interstitial collagen deposition and peri-glomerular fibrosis that was accompanied by a fibrogenic transcript signature and late post-transplant production of autoantibodies to many targets, including structural proteins including collagen IV and fibronectin. Depletion of B cells at the time DSA peak titers were achieved on day 14 post-transplant decreased serum autoantibodies levels, the kidney allograft fibrogenic transcript signature, and the chronic kidney allograft injury, despite maintenance of the high DSA titers. These results indicate a critical role for neutrophil cathepsin G during acute ABMR of kidney allografts and in its absence, DSA induced late appearance of autoantibodies mediating development of chronic kidney allograft injury.","dates":{"publication":"2026/07/06"},"accession":"GSE301384","cross_references":{"GSM":["GSM9083246","GSM9083248","GSM9083247","GSM9083249","GSM9081920","GSM9081921","GSM9081922","GSM9081900","GSM9081923","GSM9081901","GSM9081924","GSM9081902","GSM9081925","GSM9081903","GSM9081904","GSM9081926","GSM9081927","GSM9081905","GSM9081928","GSM9081906","GSM9081907","GSM9081929","GSM9081908","GSM9081909","GSM9083251","GSM9083250","GSM9081896","GSM9081930","GSM9081897","GSM9081931","GSM9081898","GSM9081910","GSM9081899","GSM9081932","GSM9081911","GSM9081912","GSM9081913","GSM9081914","GSM9081915","GSM9081916","GSM9081917","GSM9081918","GSM9081919"],"GPL":["33158","25652"],"GSE":["301384"],"taxon":["Mus musculus"]}}