Yundi Tang1, Xiaotong Sun2,3, Yuxuan Wang1, Huijie Luan4, Ruijun Zhang1, Fanlei Hu1, Xiaolin Sun1, Xia Li5, Jianping Guo6. 1. Department of Rheumatology and Immunology, Peking University People's Hospital, 11 South Xizhimen Street, Beijing, 100044, China. 2. Department of Immunology, College of Basic Medical Science, Dalian Medical University, 465 Zhongshan Road, Liaoning, 116044, China. 3. Department of Microbiology and Immunology, Medical School of Southeast University, Nanjing, 210009, China. 4. Department of Rheumatism and Immunology, Peking University Shenzhen Hospital, Shenzhen, 518036, China. 5. Department of Immunology, College of Basic Medical Science, Dalian Medical University, 465 Zhongshan Road, Liaoning, 116044, China. lixia0416@dlmedu.edu.cn. 6. Department of Rheumatology and Immunology, Peking University People's Hospital, 11 South Xizhimen Street, Beijing, 100044, China. jianpingguo@pkuph.edu.cn.
Abstract
OBJECTIVES: Interleukin (IL)-24 has been considered as an inflammatory cytokine in autoimmune diseases. However, conflicting data exist and its biological function remains controversial. Additionally, little is known about its functional impact on natural killer (NK) cells. The aim of this study was to investigate the role of IL-24 in NK cell activation and its clinical implication in systemic lupus erythematosus (SLE). METHODS: Serum cohort consisting of 299 SLE patients, 214 RA patients, and 159 healthy controls (HCs) and plasma cohort consisting of 70 SLE patients, 82 RA patients, and 123 HCs were included in evaluating IL-24 concentrations. Impact of IL-24 on NK cell activation was assessed in two NK cell subsets, i.e., CD56dimCD16+ and CD56brightCD16- NK cells. Human NK-92 cell line was applied to evaluate functional potential of IL-24 on NK cell migration and invasion. RESULTS: Serum and plasma levels of IL-24 were comparable between patients with SLE or RA and HCs. While recombinant human (rh) IL-2 consistently induced an increased expression of CD69 on both CD56dimCD16+ and CD56brightCD16- cells derived from both healthy subjects and patients with SLE, IL-24 alone was insufficient to activate the CD56dim and CD56bright NK cells. Similarly, while the migratory NK-92 cell numbers were significantly increased with rhIL-2 stimulation, IL-24 alone was unable to enhance NK-92 cell migratory and invasive capacity. CONCLUSION: Our data indicate that there were no significant differences in serum and plasma concentrations of IL-24 between SLE patients and healthy controls. Recombinant IL-24 has no effect on NK cell activation and migration. Key points • This is the first study to investigate functional potential of IL-24 on NK cell activation. • Recombinant IL-24 lacks functional capacity on NK cell activation in either CD56dimCD16+ or CD56brightCD16- NK cell subsets derived from both healthy subjects and patients with SLE. • No significant differences in serum and plasma levels of IL-24 between SLE patients and healthy controls.
OBJECTIVES: Interleukin (IL)-24 has been considered as an inflammatory cytokine in autoimmune diseases. However, conflicting data exist and its biological function remains controversial. Additionally, little is known about its functional impact on natural killer (NK) cells. The aim of this study was to investigate the role of IL-24 in NK cell activation and its clinical implication in systemic lupus erythematosus (SLE). METHODS: Serum cohort consisting of 299 SLE patients, 214 RA patients, and 159 healthy controls (HCs) and plasma cohort consisting of 70 SLE patients, 82 RA patients, and 123 HCs were included in evaluating IL-24 concentrations. Impact of IL-24 on NK cell activation was assessed in two NK cell subsets, i.e., CD56dimCD16+ and CD56brightCD16- NK cells. Human NK-92 cell line was applied to evaluate functional potential of IL-24 on NK cell migration and invasion. RESULTS: Serum and plasma levels of IL-24 were comparable between patients with SLE or RA and HCs. While recombinant human (rh) IL-2 consistently induced an increased expression of CD69 on both CD56dimCD16+ and CD56brightCD16- cells derived from both healthy subjects and patients with SLE, IL-24 alone was insufficient to activate the CD56dim and CD56bright NK cells. Similarly, while the migratory NK-92 cell numbers were significantly increased with rhIL-2 stimulation, IL-24 alone was unable to enhance NK-92 cell migratory and invasive capacity. CONCLUSION: Our data indicate that there were no significant differences in serum and plasma concentrations of IL-24 between SLE patients and healthy controls. Recombinant IL-24 has no effect on NK cell activation and migration. Key points • This is the first study to investigate functional potential of IL-24 on NK cell activation. • Recombinant IL-24 lacks functional capacity on NK cell activation in either CD56dimCD16+ or CD56brightCD16- NK cell subsets derived from both healthy subjects and patients with SLE. • No significant differences in serum and plasma levels of IL-24 between SLE patients and healthy controls.
Entities:
Keywords:
Cell activation; IL-24; NK cells subsets; Systemic lupus erythematosus