The Special Relationship in the Development and Function of T Helper 17 and Regulatory T Cells

Lochner, Matthias; Wang, Zuobai; Sparwasser, Tim

doi:10.1016/bs.pmbts.2015.07.013

Cited by 44 publications

(36 citation statements)

References 204 publications

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“…In addition, it is noteworthy that IL‐17 and RORγt, the Th17 master transcription factor, were also overexpressed. Treg and Th17 cells, which apparently exert opposite functions, as the latter are associated with pathogenic proinflammatory phenotypes, arise through a common intermediate that simultaneously up‐regulates both Foxp3 and RORγt . Tregs that constitutively express Foxp3 and RORγt have been found in human and mice and it is postulated that they can contribute to the control of exacerbated Th2 responses .…”

Section: Discussionmentioning

confidence: 99%

Hydrolysed ovalbumin offers more effective preventive and therapeutic protection against egg allergy than the intact protein

Lozano‐Ojalvo

Pérez-Rodríguez

Pablos-Tanarro

et al. 2017

Clin Experimental Allergy

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Section: Discussionmentioning

confidence: 99%

Hydrolysed ovalbumin offers more effective preventive and therapeutic protection against egg allergy than the intact protein

Lozano‐Ojalvo

Pérez-Rodríguez

Pablos-Tanarro

et al. 2017

Clin Experimental Allergy

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“…An imbalance between IL-17-producing CD4 + T helper (Th17) cells, which express the lineage-specific transcription factor, RORγt (Ciofani et al, 2012), and activated regulatory T (Treg) cells expressing Foxp3 (Gerriets et al, 2016) has a significant role in induction of inflammatory immune responses (Korn et al, 2009; Liu Y. et al, 2015; Zhu et al, 2016). This Th17/Treg imbalance is associated with various autoimmune and inflammatory diseases, including MS (Tzartos et al, 2008; Jamshidian et al, 2013, 2015; Lochner et al, 2015). An approach to suppress Th17 cell differentiation and correct Th17/Treg imbalances could be an effective treatment for chronic inflammatory diseases, such as MS.…”

Section: Introductionmentioning

confidence: 99%

MiR-384 Regulates the Th17/Treg Ratio during Experimental Autoimmune Encephalomyelitis Pathogenesis

Han

Zhang

et al. 2017

Front. Cell. Neurosci.

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Specific miRNAs are involved in the pathogenesis of multiple sclerosis (MS), during which IL-17-producing CD4+ T helper (Th17) cells accumulate in the central nervous system (CNS). In this study, we identified levels of miR-384 as significantly increased in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Over-expression of miR-384 in vivo led to severe EAE, characterized by exacerbated demyelination, and increased inflammatory cell infiltration of the spinal cord; inhibition of miR-384 reversed these changes. Both the percentage of Th17, and ratio of Th17/regulatory T (Treg), cells were elevated in miR-384-transfected EAE mice, which was consistent with the observed upregulation of expression of IL-17 and the Th17 lineage-specific transcription factor, RORγt. Importantly, transfer of miR-384 overexpressing naïve T cells from wild-type (WT) to Rag1−/− mice, which are deficient in functional autologous T and B cells, led to aggravated EAE pathogenesis, while an miR-384 inhibited group was protected from EAE. Moreover, miR-384 promoted differentiation of naïve T cells into Th17 cells in vitro. Furthermore, target prediction and dual luciferase reporter assays demonstrated that suppressor of cytokine signaling 3 (SOCS3), a gene encoding protein with an established role in Th17 differentiation, was a direct target of miR-384. Our results demonstrate an important role for miR-384 in regulation of the Th17/Treg ratio during the pathogenesis of EAE, indicating that this molecule may have potential as a biomarker and/or therapeutic target in MS.

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“…Immune disorder is an important factor associated with the pathogenesis of SSc, in particular, the impaired balance between Tregs and Th17 cells has recently been implicated in various autoimmune disorders, including SSc . Some reports previously showed that Treg cells are significantly increased in all SSc phenotypes; however, other studies revealed an increase in Th17 cells but a decrease in Treg cells in SSc with an elevated Th17/Treg ratio .…”

Section: Discussionmentioning

confidence: 99%

Effects of thalidomide on Th17, Treg cells and TGF‐β1/Smad3 pathway in a mouse model of systemic sclerosis

et al. 2019

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Objective To evaluate the immune regulatory and anti‐fibrosis function of thalidomide (Thal) in systemic sclerosis (SSc), we investigated the effects of Thal on: (a) Th17 and Treg cell production; (b) related factors expression; and (c) transforming growth factor (TGF)‐β1/Smad3 pathway, using a mouse model of SSc. Methods Forty female BALB/c mice were randomly divided into a normal control (NC) group, SSc group (bleomycin [BLM]‐induced experimental SSc), BLM + Thal (10 mg/kg/day) group, BLM + Thal (20) group, and BLM + Thal (30) group. Thal was administered a day after BLM. At the end of the animal experiments, mouse tissues were collected for detection of pathological changes and hydroxyproline content. Flow cytometry, real‐time polymerase chain reaction, enzyme‐linked immunosorbent assay, immunohistochemistry, Western blot and other methods were used to measure Th17, Treg cell population and their related factors, as well as TGF‐β1/Smad3 pathway expression. Results Thal treatment: (a) reduced skin, and pulmonary tissue fibrosis, inflammation score, and hydroxyproline content (P < .001) in BLM‐induced SSc mice; (b) reduced the percentages of Th17 cells and associated interleukin (IL)‐17A expression (both P < .05) but increased the percentages of Treg cells and its transcription factor Foxp3 expression (both P < .05); (c) correlation analysis found positive correlations between Th17/Treg ratio, the inflammatory score of the skin and pulmonary tissues, hydroxyproline content, and type I collagen messenger RNA expression (r = .8546, .8656, .6902, .6807, .8118, and .8424, respectively, P < .01); (d) Thal inhibited TGF‐β1 expression and Smad3 phosphorylation (both P < .05); (e) TGF‐β1 was positively correlated with the IL‐17A and Th17/Treg ratio (r = .5856, P = .005; r = .6684, P = .0107, respectively). Conclusion Thal can effectively prevent skin and pulmonary tissue fibrosis in a mouse model of SSc through the TGF‐β1/Smad3 signaling pathway and can rectify the distortion of the Th17/Treg balance in SSc by potentially regulating Th17 and Treg cell production, as well as their related factors expression.

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The Special Relationship in the Development and Function of T Helper 17 and Regulatory T Cells

Cited by 44 publications

References 204 publications

Hydrolysed ovalbumin offers more effective preventive and therapeutic protection against egg allergy than the intact protein

Hydrolysed ovalbumin offers more effective preventive and therapeutic protection against egg allergy than the intact protein

MiR-384 Regulates the Th17/Treg Ratio during Experimental Autoimmune Encephalomyelitis Pathogenesis

Effects of thalidomide on Th17, Treg cells and TGF‐β1/Smad3 pathway in a mouse model of systemic sclerosis

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