In vitro pharmacological modulation of NKG2D expression in immune cells from Behçet syndrome patients

Glucocorticoids, interferon-2α, colchicine, and azathioprine are recommended by EULAR for various manifestations of Behçet syndrome (BS). Curcumin is a natural compound with anti-inflammatory activities. NKG2D is a receptor expressed by NK, NKT, and CD8pos T cells implicated in recognizing stressed cells. This study aimed to: (i) evaluate the effects of selected drugs used in the management of BS plus curcumin on NKG2D expression by lymphocytes; (ii) test the effects of these drugs on immune cell subsets; and (iii) determine whether immune cells from BS patients respond differently to those from healthy controls (CTR). Peripheral blood mononuclear cells from BS patients and CTR were treated with dexamethasone, interferon-2α, colchicine, azathioprine, or curcumin for 48 h in the presence or absence of IL-15. NKG2D expression on NK, NKT, and CD8pos T cells and the percentages/absolute counts of NK, NKT, T, and B cells were evaluated by flow cytometry. All drugs down-regulated NKG2D expression. The reduction was more pronounced in CTR than in BS patients following dexamethasone treatment, in BS patients than in CTR following colchicine treatment. Dexamethasone reduced NK cells in the absence of IL-15, but increased them in its presence. Colchicine reduced B cells regardless of IL-15 stimulation. Azathioprine also down-regulated B cells, but only in the presence of IL-15 stimulation. Drugs used in the management of BS reduced NKG2D expression, potentially decreasing the activation of cytotoxic cells. Immune cells from BS patients responded differently to dexamethasone and colchicine compared to those from CTR.