Serum IL-17, IL-23, and TGF-<i>β</i>Levels in Type 1 and Type 2 Diabetic Patients and Age-Matched Healthy Controls

Roohi, Azam; Tabrizi, Mina; Abbasi, Farzaneh; Ataie‐Jafari, Asal; Nikbin, Behrouz; Larijani, Bagher; Qorbani, Mostafa; Meysamie, Alipasha; Asgarian-Omran, Hossein; Nikmanesh, Bahram; Bajouri, Arezou; Shafiey, Novin; Maleki, Akram

doi:10.1155/2014/718946

Cited by 63 publications

(48 citation statements)

References 45 publications

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“…IL-4, IL-6 and IL-13 appeared higher in diabetic groups, but no difference between EV 1 and EVwas observed. Human serum TGF-b levels were also decreased in diabetic children with either types 1 or 2 [14]. Increased levels of IL-4 and IL-6 in hyperglycaemic T1D children were found sustained even after 2 h of euglycaemia/correction [39].…”

Section: Discussionmentioning

confidence: 88%

Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes

Abdel‐Latif

Abdel-Moneim

El-Hefnawy³

et al. 2017

Clinical and Experimental Immunology

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One of the most widespread and effective environmental factors is the infection with enteroviruses (EVs) which accelerate β cell destruction in type 1 diabetes (T1D). This study represented a comparison between diabetic EV and EV children as well as correlation analysis between autoantibodies, T1D markers, cytokines, complement activation products and anti-coxsackievirus (CV) immunoglobulin (Ig)G. EV RNA was detected in Egyptian children with T1D (26·2%) and healthy controls (0%). Detection of anti-CV IgG in T1D-EV resulted in 64% positivity. Within T1D-EV , previously diagnosed (PD) showed 74 versus 56% in newly diagnosed (ND) children. Comparisons between populations showed increased levels of haemoglobin A1c (HbA1c), C-reactive protein (CRP), nitric oxide (NO), glutamic acid decarboxylase and insulin and islet cell autoantibodies [glutamic acid decarboxylase autoantibodies (GADA), insulin autoantibodies (IAA) and islet cell cytoplasmic autoantibodies (ICA), respectively], interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL -10, IL -12, IL -17, C3d and sC5-9 in T1D-EV versus T1D-EV . Conversely, both IL-20 and transforming growth factor (TGF-β) decreased in T1D-EV versus EV , while IL-4, -6 and -13 did not show any changes. Correlation analysis showed dependency of accelerated autoimmunity and β cell destruction on increased IFN-γ, IL-12 and IL-17 versus decreased IL-4, -6 and -13. In conclusion, IFN-γ, IL-12 and IL-17 played an essential role in exacerbating EV -T1D, while C3d, sC5b -9, IL-10 and -20 displayed distinct patterns.

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Section: Discussionmentioning

confidence: 88%

Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes

Abdel‐Latif

Abdel-Moneim

El-Hefnawy³

et al. 2017

Clinical and Experimental Immunology

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“…The role of IL17 on the risk for type 2 DM remains unclear. Roohi A et al [41] reported no association between serum IL17 levels and type 1 and 2 diabetes. Another study found that therapeutic improvement of glucoregulation in newly diagnosed type 2 DM patients is associated with a reduction of IL-17 levels [42].…”

Section: Discussionmentioning

confidence: 99%

Novel inflammatory markers for incident pre-diabetes and type 2 diabetes: the Rotterdam Study

et al. 2017

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The immune response involved in each phase of type 2 diabetes (T2D) development might be different. We aimed to identify novel inflammatory markers that predict progression from normoglycemia to pre-diabetes, incident T2D and insulin therapy. We used plasma levels of 26 inflammatory markers in 971 subjects from the Rotterdam Study. Among them 17 are novel and 9 previously studied. Cox regression models were built to perform survival analysis. Main Outcome Measures: During a follow-up of up to 14.7 years (between April 1, 1997, and Jan 1, 2012) 139 cases of pre-diabetes, 110 cases of T2D and 26 cases of insulin initiation were identified. In age and sex adjusted Cox models, IL13 (HR = 0.78), EN-RAGE (1.30), CFH (1.24), IL18 (1.22) and CRP (1.32) were associated with incident pre-diabetes. IL13 (0.62), IL17 (0.75), EN-RAGE (1.25), complement 3 (1.44), IL18 (1.35), TNFRII (1.27), IL1ra (1.24) and CRP (1.64) were associated with incident T2D. In multivariate models, IL13 (0.77), EN-RAGE (1.23) and CRP (1.26) remained associated with pre-diabetes. IL13 (0.67), IL17 (0.76) and CRP (1.32) remained associated with T2D. IL13 (0.55) was the only marker associated with initiation of insulin therapy in diabetics. Various inflammatory markers are associated with progression from normoglycemia to pre-diabetes (IL13, EN-RAGE, CRP), T2D (IL13, IL17, CRP) or insulin therapy start (IL13). Among them, EN-RAGE is a novel inflammatory marker for pre-diabetes, IL17 for incident T2D and IL13 for pre-diabetes, incident T2D and insulin therapy start.Electronic supplementary materialThe online version of this article (doi:10.1007/s10654-017-0236-0) contains supplementary material, which is available to authorized users.

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“…Interestingly, Th17 cells were higher in patients that presented more T2D complications[57]. Conversely, no differences were found in IL-17 plasma of T2D compared to age-matched healthy controls[61]. …”

Section: Role Of Th17 Cells In the Progression From Nafld To Nashmentioning

confidence: 99%

“…They showed higher percentages of Th17 cells in the peripheral blood in comparison with healthy lean children[61]. In other pediatric diseases these T cells were involved, principally in inflammation, such as autoimmune thyroid disease or Mycoplasma pneumoniae infection[65,66] (Table 3).…”

Section: Role Of Th17 Cells In the Progression From Nafld To Nashmentioning

confidence: 99%

Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis

Chackelevicius¹,

Gambaro²,

Tiribelli³

et al. 2016

WJG

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The nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-alcoholic steatohepatitis (NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes (Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a naïve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies.

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Serum IL-17, IL-23, and TGF-βLevels in Type 1 and Type 2 Diabetic Patients and Age-Matched Healthy Controls

Cited by 63 publications

References 45 publications

Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes

Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes

Novel inflammatory markers for incident pre-diabetes and type 2 diabetes: the Rotterdam Study

Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis

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