The CXCR5-CXCL13 axis may influence outcome in BCR-ABL1⁺ murine B-ALL and possibly human B-ALL. Percentage of GFP⁺ (BCR-ABL1⁺) BP-1⁺ cells in peripheral blood on day 27 after transplantation (P < .0001; Student t test, n = 5) (A) and Kaplan-Meier–style survival curve (B) for wild-type (WT) young recipients of 1 × 10⁶ WT (blue) or Cxcr5 knockout (KO) (red) BCR-ABL1–transduced donor bone marrow (BM) cells in the B-ALL model. The difference in survival was statistically significant (P = .0004; log-rank test, n = 11-12). (C) Representative bone sections of 2 human pediatric (left) or adult (right) patients with B-ALL stained with antibodies to CD68 labeling macrophages or CXCL13. Scale bar, 200 μm. (D) Representative bone sections of human pediatric (top) or adult (bottom) patients with B-ALL stained with antibodies to CD14 (pink) and CD16 (brown), depicting CD14^dim CD16⁺ nonclassic monocytes.²¹ The percentage of CD14^dim CD16⁺ nonclassic monocytes of all CD16⁺ monocytes/natural killer cells per patient, as counted by a blinded pathologist, is shown on the right (P = .03; Student t test, n = 4-5) The scale bar depicts 200 μm. (E) Percentage of CXCL13⁺ CD14⁺ CD16^dim (classic monocytes) vs CXCL13⁺ CD14^dim CD16⁺ (nonclassic monocytes) in BM aspirates of human pediatric patients with B-ALL (P = .0006; Student t-test, n = 4). (F) Comparison of gene expression of CXCR5 on B-ALL blasts retrieved from bone marrow (BM) at diagnosis (n = 22), BM at relapse (n = 20), and the CNS (n = 8) (ie, blast cells retrieved from cerebrospinal fluid) at CNS relapse.³⁷