IL-17A and IL-23: plausible risk factors to induce age-associated inflammation in Alzheimer’s disease

Abstract

ABSTRACTBackground: Aging and its complications such as Alzheimer’s disease (AD) are associated with chronic low-grade inflammation entitled age-associated inflammation. However, the main mechanisms whichinduce age-associated inflammation in aging and AD are yet to beclarified. L-23/IL-17A axis plays important roles in the induction of inflammation and consequently autoimmune disease. This review evaluates the main roles played by IL-17A, IL-23, and IL-17A/IL-23 axis in the pathogenesis of age-associated inflammation in AD patients.Result: IL-23/IL-17A axis, is an important factor participate in the pathogenesis of age-associated inflammation. The genetic variations and microbial infection can be considered as the most important candidates to induce AD via upregulation of IL-17A. IL-17A also deteriorates AD via induction by amyloid-β. IL-17A participates in the induction of AD by increasing neutrophils infiltration to brain, induction of neuroinflammation, increase in FASL, and amyloid-βdeposition as well as activation of microglia.Conclusions: Due to the important roles played by IL-23/IL-17A axis in AD pathogenesis, it can be considered as a target for immunotherapy against AD.Abbreviations: Aβ: β-Amyloid; AD: Alzheimer’s disease; CD: cluster of differentiation; DAMPs: Damage-associated molecular patterns; DCs: dendritic cells; HLA: human leukocyte antigen; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; RAR: retinoic-acid receptor; RORγt: RAR-related orphan receptor gamma t; SAMP8: senescence-accelerated mouse prone 8 strain; TGF-β: tumor growth factor-β; TLRs: toll-like receptors.