Contextually, IL-17A levels in γδ T cells may be directly modulated by the gut microbiota and dietary factors, reflecting their responsiveness in local microenvironments (164), while IL-17 production by Th17 cells relies on more complex regulatory mechanisms, including extracellular signals (e.g., IL-23 activation), transcription factors (e.g., RORγt), RNA, and epigenetic modifications, all of which influence their differentiation and function in the stroke microenvironment (165, 169, 170). Here, IL17A is linked to stroke disorder.