Structural insights into the activation and inhibition of CXC chemokine receptor 3

Structural insights into the activation and inhibition of CXC chemokine receptor 3

4 January 2024 | Haizhan Jiao14, Bin Pang24, Aijun Liu1, Qiang Chen1, Qi Pan13, Xiankun Wang1, Yunong Xu1, Ying-Chih Chiang1,2, Ruobing Ren1,2 & Hongli Hu1
The study investigates the structural mechanisms of activation and inhibition of CXC chemokine receptor 3 (CXCR3) by chemokines, agonists, and antagonists. CXCR3 plays a crucial role in guiding the migration and positioning of immune cells, particularly CD4+ T helper 1 (TH1) cells and CD8+ cytotoxic lymphocytes, through the interaction with chemokines CXCL9, CXCL10, and CXCL11. The structures of CXCR3 complexes with CXCL11, the peptidomimetic agonist PS372424, the biaryl-type agonist VUF11222, and the noncompetitive antagonist SCH546738 were determined using cryo-EM. The results reveal that PS372424 binds orthostatically to the N terminus of CXCL11, while VUF11222 inserts deeper into the receptor and activates CXCR3 in a distinct manner. An allosteric binding site between TM5 and TM6 was identified, which accommodates SCH546738 in the inactive state of CXCR3. The study provides insights into the activation mechanisms of CXCR3 and offers potential targets for drug development.The study investigates the structural mechanisms of activation and inhibition of CXC chemokine receptor 3 (CXCR3) by chemokines, agonists, and antagonists. CXCR3 plays a crucial role in guiding the migration and positioning of immune cells, particularly CD4+ T helper 1 (TH1) cells and CD8+ cytotoxic lymphocytes, through the interaction with chemokines CXCL9, CXCL10, and CXCL11. The structures of CXCR3 complexes with CXCL11, the peptidomimetic agonist PS372424, the biaryl-type agonist VUF11222, and the noncompetitive antagonist SCH546738 were determined using cryo-EM. The results reveal that PS372424 binds orthostatically to the N terminus of CXCL11, while VUF11222 inserts deeper into the receptor and activates CXCR3 in a distinct manner. An allosteric binding site between TM5 and TM6 was identified, which accommodates SCH546738 in the inactive state of CXCR3. The study provides insights into the activation mechanisms of CXCR3 and offers potential targets for drug development.
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