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Background Biliary tract cancer (BTC) has a poor prognosis with limited therapeutic options. γδ T cells represent an MHC-independent immune cell population; however, their therapeutic efficacy in solid tumours is constrained by insufficient tumour infiltration. Chemokine-mediated trafficking is fundamental to T lymphocyte recruitment; however, the chemokine landscape of the BTC tumour microenvironment (TME) remains uncharacterised.Objective Using single-cell RNA sequencing of BTC tissues, we delineated chemokine ligand expression patterns, stratified chemokine producers by lineage, assessed mechanisms of γδ T-cell recruitment, and identified chemokine-mediated immune escape.Methods Single-cell RNA-sequencing data from three GEO cohorts (GSE210066, GSE201425, GSE213452; 19 patients; 156,827 cells) encompassing intrahepatic, extrahepatic cholangiocarcinoma, and gallbladder malignancy were analysed using Seurat v5.0 in R. Quality control filtering applied stringent criteria (>200 genes, normal UMI counts, <15% mitochondrial content, <3% haemoglobin). Log-normalisation with technical adjustment (ribosomal and heat-shock genes removed) preceded Highly Variable Features selection (n=2,000). Harmony batch correction across datasets preceded unsupervised clustering (resolution 0.9) and UMAP visualisation. Cluster-specific markers were determined via Wilcoxon rank-sum testing using published immune and epithelial reference signatures. Chemokine expression (16 ligands; 5 receptors) was systematically quantified across all cell types using average expression and percentage expression calculations.Results Analysis of 119,840 quality-checked cells identified 27 distinct populations, including immune, epithelial, and stromal compartments. Comprehensive analysis identified a multi-axis chemokine profile, with high expression of CCL5 (30%), CXCL16 (24%), and CCL4 (23%) supporting γδ T-cell recruitment, while CCL2 and modest CXCL8 supported alternative Vδ1 T-cell axes. CXCL9 and CXCL10 expression was suppressed (<5%), thereby suppressing the IFN-γ-driven immune response. Notably, CXCL16 expression supported epithelial γδ T-cell homing via CXCR6. Paradoxically, chemokine axes supporting γδ T cell recruitment (CCL2-CCR2, CXCL8-CXCR1, CXCL12-CXCR4) simultaneously recruit immunosuppressive populations, such as myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and tumour-associated macrophages (TAMs).Conclusion Comprehensive single-cell analysis identified selective chemokine recruitment signatures supporting γδ T cell infiltration but revealed paradoxical co-recruitment of immunosuppressive populations in the BTC TME. Patient stratification via chemokine profiling combined with γδ T cell enrichment and targeted chemokine antagonism represents a rational therapeutic strategy.