Redox extracellular vesicles induce neurotoxic cytokine production from innate immune cells
نویسندگان
چکیده
Abstract Therapy induced cognition impairment (TICI) or chemobrain is a well-recognized side effect of cancer therapy, which reduces quality life for survivors. Most therapies induce reactive oxygen species, can lead to cell death, but they also promote neuronal death both directly and indirectly leading TICI. High grade gliomas are one the cancers that respond poorly therapy associated with development chemobrain. Currently, mechanisms underlying not well understood. The systemic effects such as cachexia, fatigue, cognitive sustained elevation inflammatory cytokines microglial activation. We tested hypothesis chemotherapy radiation treatment glioblastoma (GBM) leads production extracellular vesicles (EVs) oxidized proteins uniquely stimulate specific immune cells produce like TNF-α was shown by causing neurotoxicity. Previously we showed has major role in TICI, it cross blood brain barrier found induces EVs from tissues targets drugs. These contain more adducted 4-hydorxy nonenal (HNE) compared controls. released damaged therapy. HNE were better than control inducing macrophages pro-inflammatory cytokines, TNF-α, IL-6. Serum IL-6 levels producing significantly increased vivo when C57BL/6 mice injected Redox EVs. NIH R01 CA21793
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ژورنال
عنوان ژورنال: Journal of Immunology
سال: 2023
ISSN: ['1550-6606', '0022-1767']
DOI: https://doi.org/10.4049/jimmunol.210.supp.237.06