Cxcl13, also known as chemokine C-X-C motif ligand 13, is a B-cell chemokine. It binds to its receptor CXCR5, building a signaling network crucial for lymphoid neogenesis, lymphoid organization, and immune responses [1,2].

In a spinal nerve ligation (SNL) mouse model of neuropathic pain, CXCL13 was persistently upregulated in spinal cord neurons, leading to spinal astrocyte activation via CXCR5 and induction of neuropathic pain. shRNA-mediated inhibition of CXCL13 in the spinal cord attenuated SNL-induced neuropathic pain, and spinal overexpression of miR-186-5p, which suppresses CXCL13 expression, alleviated neuropathic pain. Also, neuropathic pain was abrogated in Cxcr5-/-mice [3]. In multiple myeloma, in vivo xenograft models and analysis of patient samples showed that myeloid cells were the main source of increased CXCL13 in MM-infiltrated bone marrow. CXCL13 neutralization blocked RANKL expression and osteoclast formation in vitro, and mice inoculated with CXCL13-silenced MM cells had lower bone marrow disease, reduced M2 macrophage numbers, and decreased bone disease [4].

In conclusion, Cxcl13 is essential for immune-related processes and lymphoid development. Model-based research, especially the use of KO/CKO mouse models, has revealed its role in neuropathic pain and multiple myeloma. These findings suggest that targeting Cxcl13 could be a potential therapeutic approach for these diseases.