<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/GSE319704/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</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=GSE319704</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Spatial polarization of endothelial ICAM-1 drives CD8⁺ T cell exclusion in melanoma [RNA-Seq]</name><description>An immunosuppressive tumor microenvironment (TME) constrains therapeutic efficacy and worsens prognosis. Beyond T-cell abundance and functionality, their spatial proximity to malignant cells is a critical determinant of tumor control. However, the vascular mechanisms that govern intratumoral T-cell positioning remain poorly defined. Through RNA sequencing of endothelial cells isolated from tumor cores versus peripheries in a mouse melanoma model, we identified intercellular adhesion molecule 1 (ICAM-1) as a candidate regulator of T-cell localization. As tumors progressed, T cells shifted from a balanced core–margin distribution to pronounced core exclusion, coinciding with elevated lymphocyte function-associated antigen-1 (LFA-1) expression on T cells —a pattern less evident in other immune subsets. This redistribution was accompanied by peripheral enrichment of endothelial ICAM-1 and loss of vascular integrity. Functionally, ICAM-1 blockade restored intratumoral T-cell infiltration, enhanced effector activity, and significantly delayed tumor growth. Together, these findings identify endothelial ICAM-1 as a vascular determinant of T-cell positioning and highlight the ICAM-1/LFA-1 axis as a modifiable checkpoint to improve T-cell access to the tumor core and augment antitumor immunity.</description><dates><publication>2026/09/18</publication></dates><accession>GSE319704</accession><cross_references><GSM>GSM9524114</GSM><GSM>GSM9524113</GSM><GSM>GSM9524116</GSM><GSM>GSM9524115</GSM><GSM>GSM9524118</GSM><GSM>GSM9524117</GSM><GSM>GSM9524119</GSM><GPL>34475</GPL><GSE>319704</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>