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Chemokine (C-X-C motif) ligand 13 (CXCL13), also known as B lymphocyte chemoattractant (BLC) or B cell-attracting chemokine 1 (BCA-1), is a protein ligand that in humans is encoded by the CXCL13 gene.[5][6]

Function

CXCL13 is a small chemokine belonging to the CXC chemokine family. As its other names suggest, this chemokine is selectively chemotactic for B cells belonging to both the B-1 and B-2 subsets, and elicits its effects by interacting with chemokine receptor CXCR5.[5][7] CXCL13 and its receptor CXCR5 control the organization of B cells within follicles of lymphoid tissues[8] and is expressed highly in the liver, spleen, lymph nodes, and gut of humans.[5] The gene for CXCL13 is located on human chromosome 4 in a cluster of other CXC chemokines.[6]

In T lymphocytes, CXCL13 expression is thought to reflect a germinal center origin of the T cell, particularly a subset of T cells called follicular B helper T cells (or TFH cells). Hence, expression of CXCL13 in T-cell lymphomas, such as angioimmunoblastic T-cell lymphoma, is thought to reflect a germinal center origin of the neoplastic T-cells.[9]

Role in cancer

The chemokine CXCL13 plays a dual and context-dependent role in cancer progression and the efficacy of treatments. Within the tumor microenvironment (TME), it is essential for the organization of tertiary lymphoid structures (TLS), which act as hubs for local immune activation and are typically associated with a favorable prognosis and better response to immunotherapy[10]. In contrast, elevated systemic levels of CXCL13 in the plasma have been identified as a significant biomarker of primary resistance to immunotherapy and poor clinical outcomes, especially in non-small cell lung cancer (NSCLC)[11]. High circulating levels of CXCL13 often reflect a dysregulated peripheral immune profile characterized by cytotoxic T cell exhaustion (indicated by increased markers such as LAG3 and PD-L1) and impaired B-cell maturation, which together limit the immune system’s ability to respond effectively to therapy.

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000156234 – Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000023078 – Ensembl, May 2017
  3. ^ “Human PubMed Reference:”. National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ “Mouse PubMed Reference:”. National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ a b c Legler DF, Loetscher M, Roos RS, Clark-Lewis I, Baggiolini M, Moser B (February 1998). “B cell-attracting chemokine 1, a human CXC chemokine expressed in lymphoid tissues, selectively attracts B lymphocytes via BLR1/CXCR5”. J. Exp. Med. 187 (4): 655–60. doi:10.1084/jem.187.4.655. PMC 2212150. PMID 9463416.
  6. ^ a b Gunn MD, Ngo VN, Ansel KM, Ekland EH, Cyster JG, Williams LT (February 1998). “A B-cell-homing chemokine made in lymphoid follicles activates Burkitt’s lymphoma receptor-1”. Nature. 391 (6669): 799–803. Bibcode:1998Natur.391..799G. doi:10.1038/35876. PMID 9486651. S2CID 4373691.
  7. ^ Ansel KM, Harris RB, Cyster JG (January 2002). “CXCL13 is required for B1 cell homing, natural antibody production, and body cavity immunity”. Immunity. 16 (1): 67–76. doi:10.1016/S1074-7613(01)00257-6. PMID 11825566.
  8. ^ Ansel KM, Ngo VN, Hyman PL, Luther SA, Förster R, Sedgwick JD, Browning JL, Lipp M, Cyster JG (July 2000). “A chemokine-driven positive feedback loop organizes lymphoid follicles”. Nature. 406 (6793): 309–14. doi:10.1038/35018581. PMID 10917533. S2CID 4369622.
  9. ^ de Leval L, Rickman DS, Thielen C, Reynies A, Huang YL, Delsol G, Lamant L, Leroy K, Brière J, Molina T, Berger F, Gisselbrecht C, Xerri L, Gaulard P (June 2007). “The gene expression profile of nodal peripheral T-cell lymphoma demonstrates a molecular link between angioimmunoblastic T-cell lymphoma (AITL) and follicular helper T (TFH) cells”. Blood. 109 (11): 4952–63. doi:10.1182/blood-2006-10-055145. PMID 17284527.
  10. ^ https://doi.org/10.1158/1078-0432.ccr-25-3315
  11. ^ https://doi.org/10.1186/s40364-026-00929-9