CXCR5, a G-protein coupled receptor, is essential as it binds to chemokine CXCL13, building a crucial signaling network [1,2,3]. This interaction is involved in lymphoid neogenesis, lymphoid organization, and immune responses [1]. It also has implications in multiple biological processes and diseases, making gene knockout (KO) or conditional knockout (CKO) mouse models valuable for studying its functions.

In the context of disease, CXCR5 has been implicated in numerous conditions. In autoimmune diseases like rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus, the CXCL13/CXCR5 axis is thought to play pathogenic roles, suggesting potential for CXCL13 as a biomarker and therapeutic target [1]. In neuropathic pain, spinal cord neuron-produced CXCL13 activates astrocytes via CXCR5, and in Cxcr5-/-mice, neuropathic pain is abrogated, indicating CXCR5's role in this pain mechanism [4]. In sepsis-associated encephalopathy, CXCR5 knockout in mice enhanced autophagy and partially reversed cognitive deficits induced by cecal ligation and puncture, suggesting its role in cognitive dysfunction during sepsis [5].

In conclusion, CXCR5 is vital in immune-related biological processes. Model-based research, especially through KO/CKO mouse models, has revealed its significance in various disease areas such as autoimmune diseases, neuropathic pain, and sepsis-associated encephalopathy. Understanding CXCR5's functions provides potential insights into disease mechanisms and therapeutic strategies for these conditions.