<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/GSE317nnn/GSE317860/</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=GSE317860</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Single-cell RNA-sequencing of myeloid cells in E0771 breast tumours from CD1d-KO and WT mice</name><description>Myeloid cells play crucial roles in cancer progression, influencing tumour growth, metastasis, and response to immunotherapy. Tumour-infiltrating myeloid cells are highly heterogeneous, with functions ranging from anti-tumour to tumour-promoting. The mechanisms shaping these populations remain poorly understood and may offer therapeutic opportunities. Here, we identified the lipid-presenting molecule CD1d as a regulator of tumour progression and myeloid heterogeneity in the tumour microenvironment. CD1d-deficient mice exhibit reduced tumour growth and altered immune-infiltrates in breast cancer models. Similarly, targeting CD1d with an antibody, suppresses tumour growth, reshapes the myeloid landscape, and improves anti-PD-1 immunotherapy efficacy. The CD1d-dependent control of myeloid cell functional differentiation is cell-intrinsic and conserved in human and mouse. Single-cell RNA-sequencing revealed an enhanced proinflammatory program and accumulation of inflammatory monocytes in tumours from CD1d-KO animals. Subsequently, we generated a CD1d-KO-associated gene signature that predicts clinical outcomes and response to immunotherapy in breast cancer patients. Thus, CD1d could be targeted to alter tumour-infiltrating myeloid populations and enhance immunotherapy responses.</description><dates><publication>2026/07/16</publication></dates><accession>GSE317860</accession><cross_references><GSM>GSM9480139</GSM><GSM>GSM9480138</GSM><GSM>GSM9480137</GSM><GSM>GSM9480136</GSM><GSM>GSM9480135</GSM><GSM>GSM9480134</GSM><GPL>34290</GPL><GSE>317860</GSE><taxon>Mus musculus</taxon><PMID>[42593403]</PMID></cross_references></HashMap>