Inflammatory status might direct ILC and NK cells to IL-17 expressing ILC3 and NK subsets in Behcet's disease.

Innate lymphoid cells (ILCs) are lymphoid cells that have important effector and regulatory functions in innate immunity and tissue remodeling. Uncontrolled activation and proliferation of ILCs can contribute to inflammatory autoimmune diseases. Behcet's disease (BD) is a complex systemic inflammatory disorder of unknown etiology. It has been shown that natural killer (NK) cells may play an immunoregulatory role in BD, however the role of ILCs is unknown. In this study, the levels and functions of ILCs and NK cell subsets in BD patients were investigated. Cell surface and cytotoxic granules (perforin and granzyme) expression of NK cells and ILCs were evaluated and labeled according to whole blood lysing protocol in peripheral blood samples obtained from the patients and healthy subjects. Cytokine levels of NK cells were investigated in stimulated peripheral blood mononuclear cells. All data were analyzed by flow cytometry. Total ILC and ILC3+ cells were increased in active BD patients compared to inactive BD patients and healthy subjects. There was no significant difference between the patients and healthy subjects regarding NK cell surface and intracellular molecule expression. Although, an increase in IFN-γ and IL-17, and a decrease in IL-4 levels were observed in CD56dim NK cell subset of BD patients. Recent studies showed increased neutrophilic infiltration and IL-17 secreting Th17 cells in BD patients. It is known that ILC3+cells are similar to Th17 subset regarding their cytokine profile and transcription factor expression patterns. Results of current study may suggest that inflammatory microenvironment in BD patients might direct ILC cells to differentiate into ILC3+ subset, and IL-17 released by NK cells might have a role in neutrophilic infiltration.

Follow-Up of Treatment Response With Dynamic Doppler Ultrasound in Raynaud Phenomenon.

OBJECTIVE: The purpose of this study was to investigate the role of flow parameters obtained with dynamic Doppler ultrasound in the objective follow-up of treatment response in patients with Raynaud phenomenon (RP). SUBJECTS AND METHODS: The study included 33 patients with newly diagnosed primary RP, 31 with secondary RP, and 26 healthy participants (control subjects). Both groups of patients with RP underwent sonography before and after treatment. The control group underwent sonography once. Baseline digital arterial diameter and flow volume were measured at room temperature. After cold provocation, diameter and flow volume were measured again, and flow starting time and flow normalizing time were recorded. Data were measured as mean (± SD) values. RESULTS: Baseline diameter did not significantly increase in either group after treatment (p > 0.05) (primary RP pretreatment, 0.79 ± 0.17 mm; posttreatment, 0.82 ± 0.19 mm; secondary RP pretreatment, 0.66 ± 0.13 mm; posttreatment, 0.68 ± 0.14 mm). Baseline flow volume increased significantly in both groups (p < 0.01) (primary RP pretreatment, 3.08 ± 2.96 mL/min; posttreatment, 3.91 ± 3.39 mL/min; secondary RP pretreatment, 2.14 ± 1.94 mL/min; posttreatment, 2.80 ± 2.15 mL/min). Cold provocation diameter increased significantly in both groups after treatment (p < 0.01) (primary RP pretreatment, 0.63 ± 0.15 mm; posttreatment, 0.70 ± 0.16 mm; secondary RP pretreatment, 0.56 ± 0.15 mm; posttreatment, 0.63 ± 0.13 mm). Cold provocation flow volume increased significantly in both groups after treatment (p < 0.01) (primary RP pretreatment, 1.18 ± 1.26 mL/min; posttreatment, 2.17 ± 2.16 mL/min; secondary RP pretreatment, 1.07 ± 1.40 mL/min; posttreatment, 1.46 ± 1.67 mL/min). After treatment, there was no statistically significant increase in flow starting time in patients with primary RP (p > 0.05), but there was a significant increase in patients with secondary RP (p < 0.05) (primary RP pretreatment, 1.15 ± 2.27 minutes; posttreatment, 0.61 ± 1.41 minutes; secondary RP pretreatment, 3.13 ± 4.81 minutes; posttreatment, 1.58 ± 2.36 minutes). After treatment, flow volume normalizing time improved significantly in both groups (p < 0.01) (primary RP pretreatment, 7.24 ± 7.60 minutes; posttreatment, 3.84 ± 3.39 minutes; secondary RP pretreatment, 9.58 ± 8.49 minutes; posttreatment, 4.32 ± 3.56 minutes). Among patients with primary RP, the posttreatment flow starting time was similar to that in the control group. Despite improvements, all remaining parameters differed in the treatment group compared with the control group. CONCLUSION: Doppler ultrasound can be used effectively to monitor RP treatment. Blood flow volume can be measured without cold provocation to facilitate follow-up care of patients with RP.