<p>Clear cell renal cell carcinoma (ccRCC) exhibits heterogeneity in immune infiltration and clinical outcomes, but the mechanisms governing recruitment and organization of tumor-reactive CD8⁺ T cells remain incompletely defined. We investigated the role of the CXCL13–CXCR5 axis in shaping CD8⁺ T cell recruitment, differentiation, and immune organization in high-risk, non-metastatic ccRCC. Human tumor, plasma, and matched adjacent kidney specimens were analyzed using ELISA, quantitative PCR, migration assays, multiplex immunofluorescence, single-cell RNA sequencing, spatial transcriptomics, and a syngeneic mouse model. CXCL13 was among the most upregulated chemokines in ccRCC relative to matched normal kidney and was embedded within a CD8⁺ T cell-associated inflammatory transcriptional program. In transwell and microphysiological system (MPS) assays, CXCL13 promoted CD8⁺ T cell migration, enriched CXCR5⁺ cells among migrating CD8⁺ T cells and showed reduced migration after CXCL13 or CXCR5 blockade. Single-cell analyses identified <i>CXCR5</i> expression within stem-like CD8⁺ T cell states associated with <i>TCF7</i> and <i>IL7R</i>, whereas <i>CXCL13</i> associated with later cytotoxic/exhausted states along a continuous differentiation landscape. Spatial transcriptomics demonstrated that stem-like CD8⁺ T cells localized within structured lymphoid aggregates enriched for B cells, coordinated CXCL13/CXCR5 expression, and signaling programs. In vivo, tumor-derived CXCL13 suppressed tumor growth, increased intratumoral CD8⁺ T cell infiltration, and enriched CXCR5⁺TCF1⁺CD8⁺ stem-like T cells. In human tumors, higher CXCL13 expression correlated with increased CXCR5⁺CD8⁺ T cell infiltration and improved recurrence-free survival. These findings identify CXCL13 as a regulator of immune recruitment and niche organization and support the CXCL13–CXCR5 axis as a biomarker and possible therapeutic target in ccRCC.</p>