Alteration of T helper cell subsets in the optic nerve of experimental autoimmune encephalomyelitis.

The objective of this study was to detect interleukin-17 (IL-17), interferon-gamma (IFN-gamma), interleukin-4 (IL-4) and forkhead/winged helix transcription factor p3 (Foxp3) protein and gene expression of the optic nerve and to further explore the role of T helper cell subsets such as Th1, Th2, Th17 and Treg in the pathogenesis of optic neuritis in experimental autoimmune encephalomyelitis (EAE). Mice in C57BL/6 background were randomly divided into control and EAE groups. At days 11, 15 and 19 post-immunization, optic nerves were dissected for morphological study to detect IL-17, IFN-gamma and IL-4. Protein analysis was done by enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction for measuring the gene expression of IL-17, IFN-gamma, IL-4 and Foxp3. Concentrations of IL-17 protein in the optic nerve were significantly up-regulated at 11 days post-immunization, and IFN-gamma protein concentrations at 19 days. Concentrations of IL-4 protein in the optic nerve declined slightly in 19 days. mRNA expression of IL-17, IFN-gamma and IL-4 was consistent with their protein expression. Foxp3 mRNA transcription was down-regulated at 11-19 days post-immunization. Decreased expression of Foxp3 mRNA and Treg in the optic nerve may play a key role in the development of optic neuritis. IL-17 may mediate inflammatory pathogenicity at the early stage of optic neuritis, and IFN-gamma may aggravate inflammatory injury during the peak stage of optic neuritis.