Cytokine–Microglia Interactions in Neuroinflammation: Mechanisms, Disease Dynamics, and Therapeutic Strategies

Neuroinflammation contributes to the onset and progression of a variety of central nervous system (CNS) diseases, including ischemic stroke, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, intracerebral hemorrhage, and neurodevelopmental disorders related diseases. Microglia are essential for the neurodevelopment of a healthy brain and the integrity of the blood–brain barrier. Activation of microglia is the brain’s defense mechanism against damaged tissues and harmful pathogens. However, their activation can trigger neuroinflammation, which can exacerbate or induce damage to the CNS. Cytokines are small proteins that can act in either an autocrine or paracrine manner. Cytokines are highly expressed in microglia and are potential mediators of neuroinflammation. We review the recent research progress on the role of cytokines such as interleukin-1 (IL-1β), tumor necrosis factor-α , IL-6, IL-4, and transforming growth factor-β in regulating neuroinflammation in various CNS diseases. Understanding how these cytokines affect microglia-mediated neuroinflammation will provide important therapeutic insights for preventing and managing CNS dysfunction, with potential clinical relevance for developing targeted anti-inflammatory therapies and biomarker-based diagnostic strategies. Antioxid. Redox Signal. 44, 311–331.