(A) Change in proliferating (Ki67⁺) CD4⁺ and CD8⁺ T cells (fold change postRx versus preRx) in responders (≥ VGPR; n = 19) and nonresponders (< VGPR; n = 6). (B and C) Kaplan Meier plots showing event-free survival (B) and overall survival (C) in cohorts (n = 14) based on CD4 proliferation above/below median. (D) Expression of HLADR, CD28 and FOXP3 in Ki67⁺ CD4⁺ T cells in a representative patient. (E) Ratio of increase in proliferating non-Treg CD4⁺ T cells to Treg CD4⁺ T cells posttherapy in responders (≥ VGPR) and nonresponders (< VGPR). (F) % TCE bound circulating CD4⁺ and CD8⁺ T cells in patients (54 samples) receiving weekly (n = 3), every 2 weeks (n = 21) and monthly dosing (n = 30). (G and H) Proportion of IL2 and IFN-γ secreting CD4 (G) and CD8 (H) T cells in pre and post therapy (n = 10). (I) Proportion of IL2 and IFN-γ secreting CD8⁺ T cells pre- and posttherapy specimens following stimulation with viral peptide mix against CMV, EBV, and influenza (CEF) (n =7). (J) Percent annexin V tumor cells in tumor: T cocultures in pre- and posttherapy samples (n = 12). (K and L) Impact of TCE therapy on in vivo antitumor function. (K) IVIS imaging showing tumors at day 18 (d18); Right panel shows fold change in bioluminescence at d18; (L) In situ proliferation (Ki-67⁺) of T cells at tumor site (injected bone), as analyzed by mass cytometry. Each dot is an individual sample. Bar graphs show mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Mann Whitney was used for statistical analysis in A and E. (F) Kruskall-Wallis with multiple test correction. Wilcoxon matched-pairs signed rank test was used for statistical comparisons in G–J.