CXCL8 (interleukin-8) is the most potent human neutrophil-attracting chemokine 1 that mediates inflammatory responses by recruiting neutrophils, basophils, and T cells through binding to G-protein-coupled receptors CXCR1 and CXCR2 1. Upon receptor activation, CXCL8 triggers PI3K and MAPK signaling cascades, facilitating both leukocyte chemotaxis and activation 1. Beyond acute inflammation, CXCL8 plays critical roles in disease pathogenesis. In psoriasis, IL-17A upregulates CXCL8 production in keratinocytes, driving neutrophil recruitment and perpetuating epidermal inflammation 2. In gastric cancer, tumor-associated macrophage-derived CXCL8 suppresses CD8+ T cell infiltration and induces PD-L1 expression on macrophages, promoting immune evasion 3. Similarly, in glioblastoma, hypoxia-induced CXCL8 secretion recruits immunosuppressive macrophages via ALKBH5-mediated epitranscriptomic regulation 4. Clinically, elevated CXCL8 correlates with poor prognosis in multiple cancers, and CXCR2 inhibitors like reparixin demonstrate therapeutic potential in reversing immunosuppression 35. Additionally, respiratory viruses exploit the CXCL8/MAPK/hnRNP-K axis to enhance replication 6, while radiotherapy-induced CXCL8 mobilizes cytotoxic NK cells, linking senescence to antitumor immunity 7.