Taken together, the magnitude of IL-6 serum levels could be a potential marker for arthritic manifestations and disease activity, whereas those of IFN-γ, IL-10, and IL-17cannot be considered predictors for different clinical manifestations in patients with BD.
More prominent IL-17 and IFN-γ production by all lymphocyte subsets in BD might be associated with the increased innate responses, early tissue neutrophil infiltrations and late adaptive immunity in BD.
Recently, some studies reported that Th17-associated cytokines were increased in BD; thus, Th17 cells and the IL17/IL23 pathway may play important roles in the pathogenesis of BD.
Among the PBMCs cultured with anti-CD3 and CD28 stimulation, there was an elevated secretion of TNF-α, IL-6 and IL-17 in BD patients and healthy controls with the GG genotype.
Th17 cells, mainly producing the cytokine IL-17, and Th1 cells, characterized by the production of the index cytokine IFN-γ, are the CD4(+) T lymphocyte subsets implicated in the pathogenesis of both BD and VKH.
A higher frequency of IL-17-producing CD4(+) T (Th17) cells and increased IL-17 production under Th17 polarizing conditions were observed in patients with active BD.
A significantly higher level of IL-17 was observed in the supernatants of naïve T cells and monocytes stimulated with LPS or PGN in BD patients as compared with controls.
In addition, Poly I:C supplementation could reduce inflammation through the up-regulation of memory T cells and IL-15Rα+ cells accompany with down-regulation of pro-inflammatory cytokine, IL-17A in BD mice.
The studies to date suggested that IL6, IP10 are involved in BD with nervous system lesions, IL17, IL18 are relevant to the superimposed uveitis in patients with BD.Some cytokines i.e.
We propose a model in which up-regulation of STAT4 expression and subsequent STAT4-driven production of inflammatory cytokines, such as IL-17, constitute a potential pathway leading to BD.