Th17-Mediated Immune Responses in Pathogenesis of Neuroinflammatory Disorders

Pro-inflammatory T lymphocyte populations (Th17, Th1, and Th17/1 cells) trigger and exacerbate the neuroinflammation through cytokine production and cell-cell contacts with neurons, microglial cells, and other CNS-infiltrating immune cells. A cascade of neurological injuries associated with Th17-related immune pathways arises in the CNS of patients with multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease (PD), schizophrenia, and many other autoimmune disorders. Th17 cells and their related Th subsets enhance the recruitment of neutrophils and other immune cells into the inflamed CNS which leads to irreversible neuronal damage. These events mediated via the secretion of interleukin-17 (IL-17), IL-21, IL-22, IL-23, IL-6, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and other pro-inflammatory cytokines tend to deteriorate the neuroinflammation. Therefore, it is not surprising that Th17-related responses are implicated in a wide range of neuroinflammatory and neuroimmune disorders. Here in the chapter, we have described the potential role of Th17 cells and other related pro-inflammatory Th subsets (Th1 and Th17/1) in the pathogenesis of neuroinflammatory disorders and mentioned the detailed mechanisms of neuronal injuries and apoptosis induced by Th17-associated immune responses.