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 Vol 11: Interleukin-17 impedes Schwann cell-mediated myelination.


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This article is from Journal of Neuroinflammation, volume 11.AbstractBackground: Pro-inflammatory cytokines are known to have deleterious effects on Schwann cells SCs. Interleukin 17 IL-17 is a potent pro-inflammatory cytokine that exhibits relevant effects during inflammation in the peripheral nervous system PNS, and IL-17-secreting cells have been reported within the endoneurium in proximity to the SCs. Methods: Here, we analyzed the effects of IL-17 on myelination and the immunological properties of SCs. Dorsal root ganglia DRG co-cultures containing neurons and SCs from BL6 mice were used to define the impact of IL-17 on myelination and on SC differentiation; primary SCs were analyzed for RNA and protein expression to define the putative immunological alignment of the SCs. Results: SCs were found to functionally express the IL-17 receptors A and B. In DRG cultures, stimulation with IL-17 resulted in reduced myelin synthesis, while pro-myelin gene expression was suppressed at the mRNA level. Neuronal outgrowth and SC viability, as well as structural myelin formation, remained unaffected. Co-cultures exhibited SC-relevant pro-inflammatory markers, such as matrix metalloproteinase 9 and SCs significantly increased the expression of the major histocompatibility complex MHC I and exhibited a slight, nonsignificant increase in expression of MHCII, and a transporter associated with antigen presentation TAP II molecules relevant for antigen processing and presentation. Conclusions: IL-17 may act as a myelin-suppressive mediator in the peripheral nerve, directly propagating SC-mediated demyelination, paralleled by an inflammatory alignment of the SCs. Further analyses are warranted to elucidate the role of IL-17 during inflammation in the PNS in vivo, which could be useful in the development of target therapies.



Autor: Stettner, Mark; Lohmann, Birthe; Wolffram, Kathleen; Weinberger, Jan-Philipp; Dehmel, Thomas; Hartung, Hans-Peter; Mausberg, Anne K; Kieseier, Bernd C

Fuente: https://archive.org/



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