{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE344nnn/GSE344929/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE344929"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"CD84 Determines Differential Fates of Pro-fibrotic Macrophages [scRNA-seq]","description":"Fibrotic interstitial lung diseases (fILDs) are characterized by macrophage heterogeneity and the expansion of SPP1hi pro-fibrotic macrophages. We performed single-cell RNA sequencing (scRNA-seq) of whole-lung tissues from bleomycin-treated control mice and mice with monocyte-specific Cd84 deletion to investigate how CD84 regulates myeloid cell recruitment, differentiation, and function during pulmonary fibrosis. scRNA-seq identified distinct monocyte and macrophage populations. CD84 was preferentially expressed in Spp1hi pro-fibrotic macrophages, and its expression progressively increased along the monocyte-to-pro-fibrotic macrophage differentiation trajectory. Cd84 deletion reduced the recruitment of monocyte-derived macrophages, inhibited their differentiation into Spp1hi macrophages, and shifted macrophage composition toward Il1rnhi macrophages associated with alveolar epithelial regeneration. These findings identify CD84 as a key regulator of macrophage fate and a potential therapeutic target for pulmonary fibrosis.","dates":{"publication":"2026/09/25"},"accession":"GSE344929","cross_references":{"GSM":["GSM9988151","GSM9988150","GSM9988149","GSM9988148","GSM9988147","GSM9988146","GSM9988145","GSM9988144"],"GPL":["34328"],"GSE":["344929"],"taxon":["Mus musculus"]}}