Fig. 5

Natural killer (NK) cells from patients with granulomatosis with polyangiitis (GPA) can be activated via the NK cell p30-related protein (NKp30) pathway. Peripheral blood mononuclear cells (PBMCs) were isolated and analyzed by flow cytometry as described in Fig. 2. a Dot blots showing the percentages of NKp30⁺ NK cells from healthy control subjects (HCs; n = 29) and patients with GPA (n = 28). b and c Bar graphs depicting the additive effect on degranulation of NK cells after 4-h incubation of PBMCs of patients with GPA with target cell lines. The additive effect on degranulation of NK cells from PBMCs cultured with the vector controls (VCs) shown in Fig. 4b and c is contrasted with the additive effect on degranulation after incubation with (b) BxPC-3 (n = 5; 2 active, 3 inactive) and (c) JE6-1 (n = 2; 1 active, 1 inactive) overexpressing NKp30 ligand B7-H6, respectively. The additive effect on degranulation is defined by the percentage of NK cells expressing the degranulation marker CD107a after incubation with target cells minus the percentage of NK cells expressing the degranulation marker CD107a after incubation without target cells. *Statistical significance was determined using a paired t test. d Representative histogram showing the surface expression of B7-H6 on BxPC-3 transduced with B7-H6 or the VC. B7-H6 expression on transduced JE6-1 was comparable to that on BxPC-3. IgG1 immunoglobulin G1 isotype control