Decreased interleukin-35 levels and CD4+EBI3+ T cells in patients with type 1 diabetes and the effects of the antibody against CD20 (rituximab)

Ouyang, Han; Wen, Jian Guo; Song, Kai

doi:10.5114/aoms.2020.101510

Cited by 10 publications

(8 citation statements)

References 11 publications

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“…The administration of IL-35 also reduces the number of Th1 and Th17 cells, as well as IFN-γ or IL-17Aexpressing CD8+ T cells [10]. Thereby, IL-35 plays a critical regulatory role in T1D by decreasing the in ltration of mononuclear cells in the islets [11][12].…”

Section: Full Textmentioning

confidence: 99%

Interleukin-35: A key player in chronic inflammatory Type 1 and autoimmune diabetes

Bala,

Chakraborty,

Mukherjee

2024

Preprint

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Interleukin-35 (IL-35) is a protein that was recently discovered and is composed of IL-12α and IL-27β chains. It is produced by the IL12A and EBI3 genes. Interest in the study of IL-35 has grown significantly in recent years, as evidenced by numerous scientific publications. Clinical research has revealed that patients who are negative for C-peptide have significantly lower serum levels of IL-35, which is accompanied by a decrease in the proportion of IL-35+ Treg cells, regulatory B cells, and CD8+ FOXP3+ cells that produce IL-35. This article highlights the potential importance of IL-35 expression in regulating the immune response and its role in chronic inflammatory Type 1 and autoimmune diabetes in the context of pancreatic inflammation, including its ability to control cytokine proportions, regulate B cells, and provide protection against autoimmune diabetes. Nonetheless, additional research is required to determine the exact mechanism of IL-35, and clinical trials must be carefully planned.

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Section: Full Textmentioning

confidence: 99%

Interleukin-35: A key player in chronic inflammatory Type 1 and autoimmune diabetes

Bala,

Chakraborty,

Mukherjee

2024

Preprint

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“…Singh et al noted that IL-35 + regulatory T cell frequency and plasma IL-35 concentration in patients with late autoimmune diabetes in adults (LADA) were lower than those in healthy controls [22]. Ouyang et al reported that serum levels of IL-35 in patients with T1D were lower than in healthy controls [23]. These results indicate that IL-35, expressed in local islets, can regulate the immune response of T1D by controlling the immune response of CD4 + and CD8 + T cells.…”

Section: Protection Against Diabetes Conferred By Interleukin 35mentioning

confidence: 99%

Interleukin 35: protective role and mechanism in type 1 diabetes

Zhang¹,

Liang²,

Xia³

et al. 2023

cejoi

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interleukin 35 (iL-35), a cytokine secreted by regulatory T (Treg) cells from the differentiation of conventional CD4 + T cells, is a member of the iL-12 family. The iL-12 family of cytokines exhibits an anti-inflammatory property. iL-35 has recently been shown to influence the immune modulation in various diseases, including inflammatory bowel disease, Graves' disease, rheumatoid arthritis, colitis, psoriasis, and type 1 diabetes (T1D). T1D is an immune-related disease caused by destruction of pancreatic β cells, characterized by an absolute lack of insulin. Recently, studies have suggested that protective effects of iL-35 work by improving blood glucose levels and preventing an attack of inflammatory factors on the islets. The protective mechanism may be closely related to the anti-inflammatory properties of iL-35, which include regulating macrophage phenotype, suppressing T cell proliferation, decreasing the differentiation of Th17 cells, increasing the Treg cell population, and inducing iL-35-producing regulatory T cells (iTr35). here, we review the protective effects and mechanisms of action of iL-35 in T1D.

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“…It is speculated that the decrease of neutrophils is regulated by hematopoietic factors [33] . We have found evidence that the loss of B cells will lead to the change of hematopoietic growth factors: the increase of serum B-cell activating factor (BAFF) level during B cell depletion and the change of stromalderived factor (SDF-1) concentration can regulate B cell development and regulate the outflow of neutrophils from bone marrow [57] . Figure 3 describes hematopoietic disorders associated with the pathogenesis of LON [17,49,55,[58][59][60] .…”

Section: B-cell Reconstitution After Rtb Leads To the Development Of ...mentioning

confidence: 99%

An Update on the Incidence, Risk Factors and Mechanisms of Rituximab- Associated Neutropenia

Zhang

Rao

2022

Arch Med Sci

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With the increasing application of rituximab in hematological diseases and autoimmune diseases, we have gradually increased our awareness of the adverse reaction of rituximab-associated neutropenia, but little is known about its true incidence rate, susceptibility risk factors and exact pathogenesis. At present, research groups have conducted a large number of studies on different populations. The team found that age (age > 60), advanced disease, autologous stem cell transplantation, systemic lupus erythematosus and combined cyclophosphamide therapy were independent risk factors for RAN. However, its exact mechanism is not completely clear. Several hypotheses have been put forward to solve this question, including the production of anti-neutrophil antibodies after RTB, the generation disorder and neutrophil maturation stagnation caused by abnormal B-cell reconstruction, and the amplification of T-large granular lymphocyte population that may induce neutrophil apoptosis. This article reviews the update of the incidence rate, risk factors and mechanism of RAN.

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Decreased interleukin-35 levels and CD4+EBI3+ T cells in patients with type 1 diabetes and the effects of the antibody against CD20 (rituximab)

Cited by 10 publications

References 11 publications

Interleukin-35: A key player in chronic inflammatory Type 1 and autoimmune diabetes

Interleukin-35: A key player in chronic inflammatory Type 1 and autoimmune diabetes

Interleukin 35: protective role and mechanism in type 1 diabetes

An Update on the Incidence, Risk Factors and Mechanisms of Rituximab- Associated Neutropenia

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