Correlation between serum interleukin-6 level and type 1 diabetes mellitus: A systematic review and meta-analysis

Chen, Yin-ling; Qiao, Yong-Chao; Pan, Yan-Hong; Xu, Yan; Huang, Yunxin; YinHui, Wang; Geng, Lijun; Zhao, Hai-Lu; Zhang, Xiaoxi

doi:10.1016/j.cyto.2017.01.002

Cited by 54 publications

(35 citation statements)

References 49 publications

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“…Although several reports have described a correlation between local IL-6 production and the destructiveness of pancreatic proinflammatory infiltrates in NOD mice, 62,63 data on IL-6 serum levels are inconsistent in patients with T1D. 64 Overexpression of IL-6 in local pancreatic b cells was shown to be associated with marked insulitis, accompanied by infiltration of B cells, macrophages and T cells. 63 Other findings also support the disease relevance of the IL-6 pathway, showing that STAT3 activation coordinates high expression of IL-6R in CD4 + and CD8 + T cells from patients with T1D.…”

Section: Il-6mentioning

confidence: 98%

“…Although several reports have described a correlation between local IL‐6 production and the destructiveness of pancreatic proinflammatory infiltrates in NOD mice, data on IL‐6 serum levels are inconsistent in patients with T1D . Overexpression of IL‐6 in local pancreatic β cells was shown to be associated with marked insulitis, accompanied by infiltration of B cells, macrophages and T cells .…”

Section: Classical Cytokines With Proinflammatory Rolesmentioning

confidence: 99%

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Cytokines in type 1 diabetes: mechanisms of action and immunotherapeutic targets

et al. 2020

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Cytokines play crucial roles in orchestrating complex multicellular interactions between pancreatic β cells and immune cells in the development of type 1 diabetes (T1D) and are thus potential immunotherapeutic targets for this disorder. Cytokines that can induce regulatory functions—for example, IL‐10, TGF‐β and IL‐33—are thought to restore immune tolerance and prevent β‐cell damage. By contrast, cytokines such as IL‐6, IL‐17, IL‐21 and TNF, which promote the differentiation and function of diabetogenic immune cells, are thought to lead to T1D onset and progression. However, targeting these dysregulated cytokine networks does not always result in consistent effects because anti‐inflammatory or proinflammatory functions of cytokines, responsible for β‐cell destruction, are context dependent. In this review, we summarise the current knowledge on the involvement of well‐known cytokines in both the initiation and destruction phases of T1D and discuss advances in recently discovered roles of cytokines. Additionally, we emphasise the complexity and implications of cytokine modulation therapy and discuss the ways in which this strategy has been translated into clinical trials.

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Section: Il-6mentioning

confidence: 98%

Section: Classical Cytokines With Proinflammatory Rolesmentioning

confidence: 99%

Cytokines in type 1 diabetes: mechanisms of action and immunotherapeutic targets

et al. 2020

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“…Interleukin‐6 is a pleiotropic cytokine with hormone‐like attributes that play a key role in several autoimmune and inflammatory diseases, vascular disease, metabolic abnormalities, and malignancies (Chen et al, ; Hunter & Jones, ; Narazaki, Tanaka & Kishimoto, ; Su, Lei, & Zhang, ). IL‐6 affects mitochondrial activities, the neuroendocrine system and neuropsychological behavior, and regulates the immune and inflammatory response (Hunter & Jones, ; Rohleder, Aringer, & Boentert, ).…”

Section: Introductionmentioning

confidence: 99%

The moderating role of job resources in the relationship between job demands and interleukin‐6 in an Italian healthcare organization

Falco

Corso

Girardi

et al. 2017

Research in Nursing & Health

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In this study we examined the association between job demands (JD), job resources (JR), and serum levels of a possible biomarker of stress, the pro-inflammatory cytokine interleukin-6 (IL-6). According to the buffer hypothesis of the Job Demands-Resources (JD-R) model, we expected that job resources-defined as job autonomy and social support from supervisor-might buffer the relationship between job demands, defined as emotional demands and interpersonal conflict with colleagues, and IL-6. Data from 119 employees in an Italian public healthcare organization (acute care hospital) were analyzed using multiple regression. In predicting IL-6, the interactions between emotional demands and JR and between interpersonal conflict with colleagues and job autonomy (but not social support) were significant, after controlling for the effect of age and gender. The association between JD and IL-6 was stronger for individuals with low levels of JR, so that levels of IL-6 were highest when JD were high and JR were low.Overall, these results are consistent with the buffer hypothesis of the JD-R model and also extend previous research, showing that the exposure to stressful situations at work, measured as high JD and low JR, is associated with higher levels of IL-6 in hospital employees. K E Y W O R D Sautonomy, interleukin-6, job demands, job resources, social support, work-related stress

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“…Interestingly, patients with the AKT2 E17K mutation have hypoglycemia, which is also a symptom of type I diabetes [26]. Interestingly, our EC model showed an increase in CXCL10, ICAM1, IL-6, and MIF, which are associated with type I diabetes development [27].…”

Section: Discussionmentioning

confidence: 76%

Modeling the Effects of Severe Metabolic Disease by Genome Editing of hPSC-Derived Endothelial Cells Reveals an Inflammatory Phenotype

Roudnicky

Lan

Friesen

et al. 2019

IJMS

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The kinase AKT2 (PKB) is an important mediator of insulin signaling, for which loss-of-function knockout (KO) mutants lead to early onset diabetes mellitus, and dominant active mutations lead to early development of obesity and endothelial cell (EC) dysfunction. To model EC dysfunction, we used edited human pluripotent stem cells (hPSCs) that carried either a homozygous deletion of AKT2 (AKT2 KO) or a dominant active mutation (AKT2 E17K), which, along with the parental wild type (WT), were differentiated into ECs. Profiling of EC lines indicated an increase in proinflammatory and a reduction in anti-inflammatory fatty acids, an increase in inflammatory chemokines in cell supernatants, increased expression of proinflammatory genes, and increased binding to the EC monolayer in a functional leukocyte adhesion assay for both AKT2 KO and AKT2 E17K. Collectively, these findings suggest that vascular endothelial inflammation that results from dysregulated insulin signaling (homeostasis) may contribute to coronary artery disease, and that either downregulation or upregulation of the insulin pathway may lead to inflammation of endothelial cells. This suggests that the standard of care for patients must be expanded from control of metabolic parameters to include control of inflammation, such that endothelial dysfunction and cardiovascular disorders can ultimately be prevented.

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Correlation between serum interleukin-6 level and type 1 diabetes mellitus: A systematic review and meta-analysis

Cited by 54 publications

References 49 publications

Cytokines in type 1 diabetes: mechanisms of action and immunotherapeutic targets

Cytokines in type 1 diabetes: mechanisms of action and immunotherapeutic targets

The moderating role of job resources in the relationship between job demands and interleukin‐6 in an Italian healthcare organization

Modeling the Effects of Severe Metabolic Disease by Genome Editing of hPSC-Derived Endothelial Cells Reveals an Inflammatory Phenotype

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