Circulating NK cells and their subsets in Behçet's Disease.
Clin Exp Immunol
MetadataShow full item record
Behçet's Disease (BD) is an auto-inflammatory, chronic relapsing/remitting disease of unknown aetiology with both innate and acquired immune cells implicated in disease pathogenesis. Peripheral blood Natural Killer (NK) cells and their CD56(Dim) /CD56(Bright) subsets were surface phenotyped using CD27 and CD16 surface markers in 60 BD patients compared to 60 healthy controls (HCs). Functional potential was assessed by production of interferon (IFN)-γ, Granzyme B, Perforin and the expression of degranulation marker CD107a. The effects of disease activity (BD(Active) vs. BD(Quiet) ) and BD medication on NK cells were also investigated. Peripheral blood NK cells (P < 0.0001) and their constituent CD56(Dim) (P < 0.0001) and CD56(Bright) (P = 0.0015) subsets were significantly depleted in BD patients compared to HCs and especially in those with active disease (BD(Active) ) (P < 0.0001). BD patients taking azathioprine also had significantly depleted NK cells compared to HCs (P < 0.0001). A stepwise multivariate linear regression model confirmed BD activity and azathioprine therapy as significant independent predictor variables of peripheral blood NK percentage (P < 0.001). In general, CD56(Dim) cells produced more Perforin (P < 0.0001) and Granzyme B (P < 0.01) expressed higher CD16 levels (P < 0.0001) compared to CD56(Bright) cells, confirming their increased cytotoxic potential with overall higher NK cell CD107a expression in BD compared to HCs (P < 0.01). Interestingly, IFN-γ production and CD27 expression were not significantly different between CD56(Dim) /CD56(Bright) subsets. In conclusion, both BD activity and azathioprine therapy have significant independent depletive effects on the peripheral blood NK cell compartment. This article is protected by copyright. All rights reserved.