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• W2914272877 startingPage "139" @default.
• W2914272877 abstract "Increasing evidence suggests that T cells participate in the pathology of neuropathic pain, as well as the activation of microglia. However, whether T cells infiltrate into the spinal cord and contribute to the development of bone cancer pain (BCP) remains unknown. Here, we used a mouse model of BCP to show that numbers of T cells infiltrated into the spinal cord after sarcoma cell implantation with increased BCP, and most infiltrating T cells in the spinal cord were CD3+CD4+ T cells. Both Th17 and Treg subpopulations were analyzed by immunofluorescence. Treg cells in the spinal cord were transiently up-regulated, followed by an imbalance towards Th17 afterwards, and elevated IL-17/IL-17A levels were observed in both blood and spinal cord. Meanwhile, TGF-β, IL-6, and IL-23, the factors which regulate Th17/Treg differentiation, increased their expressions during the development of BCP. Additionally, IL-17A receptor (IL-17AR) was found to be expressed on microglia, and the level of IL-17AR increased with activated microglia during BCP development. Furthermore, BCP was ameliorated when IL-17/IL-17A neutralizing antibodies were intrathecally injected, accompanied with inhibited Th17/Treg infiltration and suppressed microglial activation. In conclusion, T cells infiltrated into the spinal cord with the imbalance of Th17/Treg towards Th17 during the development of BCP, which could promote the microglial activation and further increased BCP, while neutralizing IL-17/IL-17A in the spinal cord could ameliorate BCP. Our results suggest that targeting the imbalanced Th17/Treg infiltration in the spinal cord could be a novel strategy for BCP therapy." @default.
• W2914272877 created "2019-02-21" @default.
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• W2914272877 date "2019-07-01" @default.
• W2914272877 modified "2023-10-14" @default.
• W2914272877 title "Imbalanced spinal infiltration of Th17/Treg cells contributes to bone cancer pain via promoting microglial activation" @default.
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• W2914272877 doi "https://doi.org/10.1016/j.bbi.2019.01.024" @default.
• W2914272877 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30685532" @default.
• W2914272877 hasPublicationYear "2019" @default.
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