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These interactions involve a wide spectrum of pathogenic mechanisms, including immune dysregulation 6 and the hyperactivation of some proinflammatory cytokines and chemokines, such as interleukin-6 (IL-6), chemokine ligand 1 (CXCL1/KC), macrophage inflammatory protein-1 alpha (CCL3/MIP-1) and monocyte chemoattractant protein-1 (CCL2/MCP-1) 7