The heightened infection risk in GD may be attributable to dysfunction of immune cells, including monocytes, macrophages, dendritic cells, T cells, and B cells, as well involvement of cytokines, such as MCP1/CCL2, CXCL8/IL8, CXCL1, IL-1β, IFNγ, and TNFα, are implicated in GD progression (45–50). This evidence concerns the gene CCL2 and infection.