IL-17A and IFN-? are Up-regulated in CD4 and ?d T Cells in Active Behcet's Disease Patients

Involvement of gamma delta T cells is implicated in the pathogenesis of Behcet's disease (BD) as a bridge between innate and adaptive responses. IL-17 and IL-22 have also been shown to participate in the BD pathogenesis in addition to IFN-gamma. Mainly CD4(+) T cells are investigated previously for the production of these inflammatory cytokines. In this study, the role of gamma delta T cells in cytokine-related mechanisms was evaluated in BD in comparison to CD4(+) T cells. Surface expression of markers for functional states of both CD4(+) and gamma delta T cells were compared in ex vivo samples collected from patients with BD and healthy controls (HC).& nbsp;Sixteen active BD (a-BD), 9 inactive BD (i-BD) patients and 25 HC were investigated. The expression of CD161, CCR6 as markers for IL-17 producing cells were analyzed on gamma delta and CD4(+) T cells. IFN-gamma, IL-17A, IL-22, as well as CD107a (LAMP1) and CD16 (Fc gamma RIII) were evaluated in both cell subtypes after in vitro stimulation.& nbsp;Only IFN-gamma production was increased in gamma delta T cells of a-BD patients. There was no difference in increase of CD107a or decrease of CD16 surface expression on gamma delta T cells upon stimulation between the groups. Ex vivo IL-17A and both IL-17A/IFN-gamma production and expression of CD161, CCR6 by CD4(+) T cells were increased in a-BD.& nbsp;Along with CD4(+) T cells, gamma delta T cells have complementary roles in cytokine production in BD. Higher IFN-gamma production of gamma delta T cells suggests the role of an environmental triggers in BD pathogenesis, whereas IL-17 related activity is mainly provided by CD4(+) T cells.

Automated summary

Gamma delta T cells and CD4(+) T cells have complementary roles in cytokine production in Behcet's disease. The higher IFN-gamma production of gamma delta T cells suggests the role of environmental triggers in Behcet's disease pathogenesis, while IL-17 related activity is mainly provided by CD4(+) T cells.