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To exclude the possibility that IL18R1 recruitment through signaling pathway activation is mediated by CXCL10 and CXCR# binding, we selected CXCR2 and CXCR4 that show higher binding affinity to CXCL10 than to other CXCR members through AlphaFold, and set up CTR versus CXCL10 versus CXCL10 + CXCR3 Ab (antibody) versus CXCL10 + CXCR2 Ab versus CXCL10 + CXCR4 Ab, and found that none of these three antibodies treatment rescues the increased level of p-JNK, P-AKT, and p-P65

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