<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/GSE319nnn/GSE319886/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319886</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>ICAM1 expression and associated clinical parameters as predictive biomarkers for acute celluar rejection</name><description>Background: Acute cellular rejection (ACR) remains a significant complication after liver transplantation (LT). To identify pre-transplant biomarkers and elucidate the underlying immune mechanisms predisposing recipients to ACR, LT recipients were enrolled. Methods: Clinical parameters were analyzed pre- and post-LT. Single-cell RNA sequencing (scRNA-seq) was performed on pre-LT liver biopsies to characterize the immune microenvironment. Functional assays were performed in vitro and in vivo. Results: Pre-LT hepatitis virus infection was an independent risk factor for ACR. scRNA-seq revealed a distinct pre-LT immune landscape in patients who developed into ACR with a reduced proportion of T/NK cells but an enrichment of highly cytotoxic NK subsets (e.g., NK⁺_GNLY⁺), which was associated with downregulation of key adhesion molecules, particularly the ICAM1-ITGB2 (LFA-1) axis. ICAM1 knockdown impaired macrophage migration and synapses formation in vitro and suppressed the MAPK-ERK pathway. Clinically, low intrahepatic ICAM1 expression pre-LT correlated with diminished leukocyte infiltration (CD45⁺, CD18⁺), increased post-transplant collagen deposition, and more severe ACR. Furthermore, recipient ICAM1 levels strongly correlated with distinct serum parameter profiles, negatively with early post-LT ALT and positively with pre-LT bilirubin levels. Conclusion: Results suggest that a pre-LT state of dysregulated cytotoxicity and impaired immune cell adhesion/migration, characterized by low ICAM1 expression and a suppressed MAPK pathway, predisposes patients to ACR. ICAM1 expression, combined with specific bilirubin and liver enzyme profiles, emerges as a promising integrated biomarker for predicting rejection risk.</description><dates><publication>2026/06/30</publication></dates><accession>GSE319886</accession><cross_references><GSM>GSM9528637</GSM><GSM>GSM9528636</GSM><GSM>GSM9528635</GSM><GSM>GSM9528634</GSM><GSM>GSM9528633</GSM><GSM>GSM9528632</GSM><GPL>24676</GPL><GSE>319886</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>