<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301384/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by array</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301384</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Nanostring gene expression profiling in a mouse model of antibody-mediated rejection of kidney allografts</name><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.</description><dates><publication>2026/07/06</publication></dates><accession>GSE301384</accession><cross_references><GSM>GSM9083246</GSM><GSM>GSM9083248</GSM><GSM>GSM9083247</GSM><GSM>GSM9083249</GSM><GSM>GSM9081920</GSM><GSM>GSM9081921</GSM><GSM>GSM9081922</GSM><GSM>GSM9081900</GSM><GSM>GSM9081923</GSM><GSM>GSM9081901</GSM><GSM>GSM9081924</GSM><GSM>GSM9081902</GSM><GSM>GSM9081925</GSM><GSM>GSM9081903</GSM><GSM>GSM9081904</GSM><GSM>GSM9081926</GSM><GSM>GSM9081927</GSM><GSM>GSM9081905</GSM><GSM>GSM9081928</GSM><GSM>GSM9081906</GSM><GSM>GSM9081907</GSM><GSM>GSM9081929</GSM><GSM>GSM9081908</GSM><GSM>GSM9081909</GSM><GSM>GSM9083251</GSM><GSM>GSM9083250</GSM><GSM>GSM9081896</GSM><GSM>GSM9081930</GSM><GSM>GSM9081897</GSM><GSM>GSM9081931</GSM><GSM>GSM9081898</GSM><GSM>GSM9081910</GSM><GSM>GSM9081899</GSM><GSM>GSM9081932</GSM><GSM>GSM9081911</GSM><GSM>GSM9081912</GSM><GSM>GSM9081913</GSM><GSM>GSM9081914</GSM><GSM>GSM9081915</GSM><GSM>GSM9081916</GSM><GSM>GSM9081917</GSM><GSM>GSM9081918</GSM><GSM>GSM9081919</GSM><GPL>33158</GPL><GPL>25652</GPL><GSE>301384</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>