Aberrant IL ‐35 levels in patients with primary Sjogren's syndrome

2020

BMC Immunol

Background: Interleukin-35 (IL-35) is a newly identified IL-12 cytokine family member, which regulates the activity of immune cells in infectious diseases and autoimmune disorders. However, the regulatory function of IL-35 in Kawasaki disease is not well elucidated. Methods: Thirty-three patients with Kawasaki disease and seventeen healthy controls were studied. Peripheral IL-35 concentration was measured by enzyme linked immunosorbent assay. CD14 + monocytes were purified, and mRNA expression of IL-35 receptor (IL-12Rβ2 and gp130) was semi-quantified by real-time polymerase chain reaction. CD14 + monocytes were stimulated with recombinant IL-35. The modulatory role of IL-35 treated CD14 + monocytes to naïve CD4 + T cell activation was investigated by flow cytometry. The influence of IL-35 to cytotoxicity of CD14 + monocytes was assessed by measuring target cell death, cytokine and granzyme secretion.Results: Plasma IL-35 concentration was elevated in patients with Kawasaki disease. There was no significant differences of either IL-12Rβ2 or gp130 mRNA expression in CD14 + monocytes between Kawasaki disease patients and controls. IL-35 suppressed CD14 + monocytes induced naïve CD4 + T cell activation in Kawasaki disease, and this process required direct cell-to-cell contact. IL-35 also inhibited tumor necrosis factor-α and granzyme B secretion by CD14 + monocytes from patients with Kawasaki disease, however, only granzyme B was responsible for the cytotoxicity of CD14 + monocytes.Conclusions: IL-35 played an important immunosuppressive role to CD14 + monocytes function in Kawasaki disease.

Section: Discussionmentioning

confidence: 69%

Increased Interleukin-35 suppresses peripheral CD14+ monocytes function in patients with Kawasaki disease

2020

BMC Immunol

“…There were no remarkable differences of either FasL or TRAIL mRNA level between cell with and without IL-35 stimulation (paired t tests, p>0.05, Figure 3g and 3h). Decreased expression of peripheral IL-35 was reported in patients with systemic lupus erythematosus [24], multiple sclerosis [25], primary Sjogren's syndrome [26], and psoriasis vulgaris [27]. In contrast, intestinal regulatory B cells and circulating regulatory CD4 + /CD8 + T cells produced high level of IL-35 in active inflammatory bowel disease [28].…”

Section: In Vitro Il-35 Stimulation Suppressed Cd14 + Monocytes Mediamentioning

confidence: 99%

Increased Interleukin-35 Suppresses Peripheral CD14+ Monocytes Function in Patients with Kawasaki Disease

2020

Preprint

Background Interleukin-35 (IL-35) is a newly identified IL-12 cytokine family member, which regulates the activity of immune cells in infectious diseases and autoimmune disorders. However, the regulatory function of IL-35 in Kawasaki disease is not well elucidated. Methods Thirty-three patients with Kawasaki disease and seventeen healthy controls were studied. Peripheral IL-35 concentration was measured by enzyme linked immunosorbent assay. CD14 + monocytes were purified, and mRNA expression of IL-35 receptor (IL-12Rβ2 and gp130) was semi-quantified by real-time polymerase chain reaction. CD14 + monocytes were stimulated with recombinant IL-35. The modulatory role of IL-35 treated CD14 + monocytes to naïve CD4 + T cell activation was investigated by flow cytometry. The influence of IL-35 to cytotoxicity of CD14 + monocytes was assessed by measuring target cell death, cytokine and granzyme secretion. Results Plasma IL-35 concentration was elevated in patients with Kawasaki disease. There was no significant differences of either IL-12Rβ2 or gp130 mRNA expression in CD14 + monocytes between Kawasaki disease patients and controls. IL-35 suppressed CD14 + monocytes induced naïve CD4 + T cell activation in Kawasaki disease, and this process required direct cell-to-cell contact. IL-35 also inhibited tumor necrosis factor-α (TNF-α) and granzyme B secretion by CD14 + monocytes from patients with Kawasaki disease, however, only granzyme B was responsible for the cytotoxicity of CD14 + monocytes. Conclusions IL-35 played an important immunosuppressive role to CD14 + monocytes function in Kawasaki disease.

“…Decreased expression of peripheral IL-35 was reported in patients with systemic lupus erythematosus [24], multiple sclerosis [25], primary Sjogren's syndrome [26], and psoriasis vulgaris [27]. In contrast, intestinal regulatory B cells and circulating regulatory CD4 + /CD8 + T cells produced high level of IL-35 in active inflammatory bowel disease [28].…”

Section: Recent Studies Have Revealed Abnormal Expression Of Il-35 Inmentioning

confidence: 99%

Increased Interleukin-35 Suppresses Peripheral CD14+ Monocytes Function in Patients with Kawasaki Disease

2019

Preprint

Background: Interleukin-35 (IL-35) is a newly identified IL-12 cytokine family member, which regulates the activity of immune cells in infectious diseases and autoimmune disorders. However, the regulatory function of IL-35 in Kawasaki disease is not well elucidated.Methods: Thirty-three patients with Kawasaki disease and seventeen healthy controls were studied. Peripheral IL-35 concentration was measured by enzyme linked immunosorbent assay. CD14+ monocytes were purified, and mRNA expression of IL-35 receptor (IL-12Rβ2 and gp130) was semi-quantified by real-time polymerase chain reaction. CD14+ monocytes were stimulated with recombinant IL-35. The modulatory role of IL-35 treated CD14+ monocytes to naïve CD4+ T cell activation was investigated by flow cytometry. The influence of IL-35 to cytotoxicity of CD14+ monocytes was assessed by measuring target cell death, cytokine and granzyme secretion.Results: Plasma IL-35 concentration was elevated in patients with Kawasaki disease. There was no significant differences of either IL-12Rβ2 or gp130 mRNA expression in CD14+ monocytes between Kawasaki disease patients and controls. IL-35 suppressed CD14+ monocytes induced naïve CD4+ T cell activation in Kawasaki disease, and this process required direct cell-to-cell contact. IL-35 also inhibited tumor necrosis factor-α (TNF-α) and granzyme B secretion by CD14+ monocytes from patients with Kawasaki disease, however, only granzyme B was responsible for the cytotoxicity of CD14+ monocytes.Conclusions: IL-35 played an important immunosuppressive role to CD14+ monocytes function in Kawasaki disease.