{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315637/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":[" Other","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315637"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Immunopeptidome profiling in pulmonary fibrosis provides a new platform for identifying therapeutic targets","description":"Fibrosis is the common and final pathological outcome of many chronic diseases and is a significant unmet medical need. Changes in the peptide profile presented by major histocompatibility complex class I molecules (MHC-I) are important pathological signals in diseases. The identification of \"new antigens\" in fibrosis potentially helps understand the pathogenesis and the therapeutic target. Here, we show that characterizing the MHC-I immunopeptidome of pulmonary fibrosis tissues identifies a series of pathological MHC-I ligands, leading to the discovery of multiple \"fibrosis-associated antigens (FAAs)\". Notably, three MHC-I peptides from Tns3, Apbb2, and Maf effectively block pulmonary fibrosis progression when used as a therapeutic vaccine. This study shows that profiling the immunopeptidome in fibrotic disease provides a promising platform for identifying therapeutic targets.","dates":{"publication":"2026/05/07"},"accession":"GSE315637","cross_references":{"GSM":["GSM9433608","GSM9433619","GSM9433609","GSM9433617","GSM9433618","GSM9433607","GSM9433615","GSM9433616","GSM9433613","GSM9433614","GSM9433622","GSM9433611","GSM9433612","GSM9433620","GSM9433621","GSM9433610"],"GPL":["24247","34290"],"GSE":["315637"],"taxon":["Mus musculus"],"PMID":["[42010059]"]}}