Ed with these properties. MHCI was detected mainly in the cytoplasm, and the expression was increased by IL-17 in a dose-dependent manner. Compared with MHCI, MHCII revealed a fainter basic expression and also an increase in protein expression after IL-17, with a significantly increased expression at 0.5 ng/mL IL-17, whereas 50 ng/mL just revealed a tendency without statistical significance. Antigenic peptides are transferred to the endoplasmic reticulum PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28151467 by TAP. We found that the expression of TAPII increased slightly in a dose-dependent manner following IL-17 treatment, but without statistical significance in densitometric analysis. Thus, we assume that the capacity of SCs to HIV-1 integrase inhibitor 2 web activate CD8+ and CD4+ T cells, and therefore to act as antigenpresenting cells in a condition of inflammation, was increased. In accord with our findings, SCs express major histocompatibility complex molecules and increase the expression of these molecules under pro-inflammatory conditions in vivo and in vitro [17,18,58-70]. Whether the change of MHCII and TAP expression in SC after IL-17 stimulation is functional is notional. The results warrant further functional analysis of MHCII expression in SCs. Corroborating our results, regulated expression of the intracellular antigen-processing machinery in peripheral nerve sections from GBS patients was recently shown (Meyer zu Horste et al. [17]), and SCs most likely act as non-professional antigen-presenting cells under certain conditions. The IL-17-induced increased expression can be interpreted as an immunological alignment of SCs. This modulation of SC homeostasis by inflammatory mediators was reported for interleukins, iNOS, COX-2, and MMPs as a response to the surrounding environment [20-24]. IL-17 led to no reduction of SC viability, showed no effect on NF expression, and did not change the structural myelin formation, but significantly interfered with SC-mediated myelination. Negative regulators of myelination which do not necessarily initiate apoptosis such as c-Jun, Notch, Sox-2, Pax-3, Id2, Krox-24, and Egr-3 are known. They are found downregulated after initiation of myelination and may be reactivated after PNS injury causing SC dedifferentiation [41]. Further inflammatory mediators, such as TNF-, can promote phenotype reversion of mature to immature SCs [25-27,41]. It was suggested before that negative regulators of SCmyelination may foster neuronal survival and axonal regrowth but actively suppress myelination. In the context of neuropathies, such pathways may cause further harm [41].does not appear to involve an indirect effect caused by either a reduced neuronal stimulus for myelination or a toxic effect, but rather a direct reprogramming of SC differentiation. This latter effect may contribute to Wallerian degeneration and equipping of the inflammatory facilities of SCs in order to modulate the process of inflammation. These data provide new insights into the role of IL-17 in the inflammatory response in the PNS that could be useful in the development of targeted therapies.Abbreviations AU: arbitrary unit; AX: axon; CIDP: chronic inflammatory demyelinating polyneuropathy; CSF: cerebrospinal fluid; DAPI: diamidino-2-phenylindole; DMEM: Dulbecco’s modified eagle’s medium; DRG: dorsal root ganglia; FCS: fetal calf serum; FKS: forskolin; GAPDP: glyceraldehyde 3-phosphate dehydrogenase; GBS: Guillain-Barr?syndrome; Glut: L-glutamine; HBSS: Hank’s balanced salt solution; HEPES: 4-(2-hydroxyethyl)-1-piperazi.