Ccr7, a chemokine receptor, is a G protein-coupled receptor with 7 transmembrane domains. It plays a crucial role in immune cell trafficking, being expressed on various cells like naive T/B cells, central memory T cells, etc. Ccr7, along with its ligands CCL19 and CCL21, is involved in the migration of dendritic cells to T-cell zones in lymph nodes, initiating antigen presentation and T-cell response. It also participates in the CCL21/CCR7 axis, which is associated with autoimmune diseases, cancer metastasis, and other pathological conditions [1,2,4,5].

In autoimmune diseases such as rheumatoid arthritis, sjogren's syndrome, etc., genome-wide association studies have shown a strong link between the CCL21/CCR7 axis and disease severity. Disrupting the CCL21/CCR7 interaction can prevent the migration of CCR7-expressing cells to the site of inflammation and reduce disease severity [1]. In cancer, the CCR7 axis has a dual role. It can contribute to the trafficking of effector cells for anti-tumor immune responses, but also plays a role in tumor cell migration towards the lymphatic system and metastasis [2]. In blood cancers, CCR7 expression often correlates with nodal or spleen involvement [3].

In conclusion, Ccr7 is essential for immune cell migration and the regulation of immune responses. Its role in autoimmune diseases and cancer, as revealed through various studies, highlights its potential as a therapeutic target. Understanding Ccr7's functions through model-based research, especially in the context of these diseases, can provide new strategies for treatment and management.