For this purpose, we evaluated in vivo and ex vivo IL-18, interferon-γ (IFN-γ) levels using ELISA and NO production by the Griess' method in naïve-active and corticosteroid-treated BD patients with different clinical manifestations.
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.
Decreased expression of GAS6 and increased pro-inflammatory cytokines (IL-6 and IFN-γ: P = 4.23 × 10(-4), P = 0.011, respectively) in individuals carrying the CC genotype suggest that the TAM-GAS6/PROS1 signal pathway may be involved in the pathogenesis of BD.
However, there was no significant change in secretion of IFN- γ in BD patients and healthy controls among the genotype of this IL-23R gene polymorphism.
To examine the role of IL-28A in the pathogenesis of BD, we measured the expression of IFN-γ and IL-17 by IL-28A-stimulated peripheral blood mononuclear cells (PBMCs) from 19 patients with BD and 16 healthy individuals.
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.
Similarly, levels of IL-17, IL-23, IL-12/23p40, and IFN-γ in serum and supernatants were significantly elevated in patients with BD despite the fact that IL-12p35 and IL-12/23p40 mRNA expression in PBMCs was up-regulated in the inactive BD group.
Collectively, we found excessive CD4(+) T cells producing IL-17 and IFN-γ (Th1/Th17) cells in patients with BD, and possible involvement of IL-23/IL-23R pathway for the appearance of excessive Th1/Th17 cells.
In patients with similar disease activity, levels of IL-15 and IFN-γ were significantly higher in BD patients than in VKH and HLA-B27-associated uveitis groups.
The aim of the current study was to define the expression on CD3+ T cells of six chemokine receptors associated with inflammatory sites and the expression of intracellular cytokines, such as interferon-gamma (IFN-gamma) and interleukin-4 (IL-4), in Behcet's disease (BD).
We observed important increases in the expression of interleukin-8 (IL-8) ( approximately 700-fold), monocyte chemoattractant protein 1 ( approximately 65-fold), interferon-gamma ( approximately 71-fold), and IL-12 ( approximately 69-fold) messenger RNA in BD lesions compared with normal skin.