Th17 and Treg Cells in Bone Related Diseases

Wang, Min; Tian, Tian; Yu, Shuang; He, Na; Ma, Daoxin

doi:10.1155/2013/203705

Cited by 37 publications

(41 citation statements)

References 103 publications

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“…23 The role of Treg/Th17 response in inflammatory immune bone resorption has been explored in other diseases. 26 In rheumatoid arthritis (RA), studies describe an excessive production of IL-17 followed by bone and cartilage destruction. Moreover, Treg in RA are not entirely efficient to control inflammation.…”

Section: Summary Of Evidencementioning

confidence: 99%

Treg and Th17 cells in inflammatory periapical disease: a systematic review

et al. 2017

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The process involved in periapical lesions, which occur as an outcome of pulpal necrosis, is regulated by the immune system including regulatory T cells (Treg) and T helper 17 cell (Th17) responses. The objective of this study was to conduct a frequency systematic review to determine the presence of Treg/Th17 responses and the influence of these cells in the progression of chronic inflammatory periapical lesions in humans. A systematic computerized search was carried out in Pubmed, Medline, Web of Science and Scopus electronic databases from their date of inception through the first week of May 2017. In addition, the reference lists of the included articles and the grey literature were hand-searched. Articles that evaluated the presence and influence of Treg/Th17 in the progression of human periapical lesions were included. Study selection and the quality assessment of the included articles (using the Newcastle-Ottawa scale) were carried out by two authors. Fifty-seven titles/abstracts were screened and eight studies met the eligibility criteria and were included in this systematic review. The included studies showed large variation in the type of periapical lesion assessed, mean age, age range, type of experiment and findings regarding the participation of Th17 and Treg in the status of inflammatory periapical lesions. The studies showed the involvement of Treg in the modulation of the inflammatory response in radicular cysts and periapical granulomas. This systematic review highlights the relationship between Treg and Th17 acting in a subtle balance inhibiting or promoting the progression of human periapical lesions.

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Section: Summary Of Evidencementioning

confidence: 99%

Treg and Th17 cells in inflammatory periapical disease: a systematic review

et al. 2017

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“…Treg cells participate in fracture healing mainly through three mechanisms: (1) expressing cytotoxic T lymphocyte antigen-4 (CTLA-4) on the surface of cells directly contacting with target cells to inhibit the damage of inflammatory cells to bone tissue, (2) promoting osteoblast activity while inhibiting osteoclast activity, and (3) producing cytokines such as TGFbeta and IL-10 [21][22][23]. Activated Th17 cells regulate fracture healing mainly through the following three ways: (1) enhancing the expression of IL-17 in the fracture site, (2) enhancing the activity of osteoclasts, and (3) blocking the formation of osteoblasts and inhibiting the activity of osteoblasts [21][22][23]. We speculate that the A2A receptor agonist can regulate the above cell balance in a rat fracture model.…”

Section: Introductionmentioning

confidence: 99%

The Adenosine A2A Receptor Agonist Accelerates Bone Healing and Adjusts Treg/Th17 Cell Balance through Interleukin 6

Zheng

Wang

2020

BioMed Research International

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The aim of this study was to explore the effect of adenosine A2A receptor agonists on fracture healing and the regulation of the immunity system after bone fracture. We implanted fibrin gel containing adenosine A2A receptor agonist CGS 21680/inhibitor ZM 241385/saline locally in rat tibial fracture models, finding that the adenosine A2A receptor agonist could promote fracture healing. At the same time, the adenosine A2A receptor agonist decreased the level of IL-6 in blood and the fracture area, increased Treg cells, and decreased Th17 cells in blood of bone fracture rats. Further, tibial fracture rats implanted with the adenosine A2A receptor agonist gel were injected with IL-6. We found that IL-6 could reverse the effect of adenosine A2A receptor agonists on fracture healing and Treg/Th17 cells in blood. Through the above results, we believe that the adenosine A2A receptor agonist can promote fracture healing and regulate Treg/Th17 cells in blood of rats with fractures. These effects are related to IL-6.

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“…in these diseases [19]. Under inflammatory conditions, MSCs mediate the adhesion of Th17 cells via CCR6 and exert anti-inflammatory effects through the induction of a Treg phenotype in these cells [10].…”

Section: Discussionmentioning

confidence: 99%

SOST Gene Inhibits Osteogenesis from Adipose-Derived Mesenchymal Stem Cells by Inducing Th17 Cell Differentiation

Chen

Pan

et al. 2018

Cell Physiol Biochem

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Background/Aims: Postmenopausal osteoporosis is considered to be an autoimmune and inflammatory process, and IL-17 plays important roles in the loss of bone mass. Sclerostin (SOST) acts as a negative regulator of bone formation by inhibiting the Wnt signaling pathway. It also is a mediator of the crosstalk between the skeletal and immune systems. However, few studies have examined the role of SOST gene in the differentiation of T helper 17 (Th17) cells. Methods: Adipose-derived stem cells (ADSCs) were isolated and transfected with pcDNA3-SOST or shSOST, and then co-cultured with CD4⁺ T cells isolated from peripheral blood mononuclear cells. The differentiation, adipogenesis, and osteogenesis of Th17 and regulatory T (Treg) cells were examined by western blot, intracellular and intranuclear staining, ELISA, and real-time quantitative PCR in this co-culture model. Results: The SOST gene promoted the secretion of IL-6 and TGF-β in ADSCs. After co-culture of ADSCs with CD4⁺ T cells, the SOST gene increased the number of CD4⁺IL-17⁺ cells and the levels of IL-17 and RORγ. However, the number of CD4⁺CD25⁺Foxp3⁺ cells was decreased, which was accompanied with a reduction of IL-10 and Foxp3 expression. In the meantime, the SOST gene inhibited the expression of COL1, OCN, and OPN, reduced the activity of alkaline phosphatase, and increased the expression of LPL and PPARγ. Furthermore, IL-17 promoted SOST gene-induced adipogenesis and increased the inhibition of osteogenesis. Conclusions: SOST promoted the differentiation of Th17 cells and reduced the differentiation of Treg cells, which exacerbated the SOST gene-induced inhibition of osteogenesis from ADSCs.

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Th17 and Treg Cells in Bone Related Diseases

Cited by 37 publications

References 103 publications

Treg and Th17 cells in inflammatory periapical disease: a systematic review

Treg and Th17 cells in inflammatory periapical disease: a systematic review

The Adenosine A2A Receptor Agonist Accelerates Bone Healing and Adjusts Treg/Th17 Cell Balance through Interleukin 6

SOST Gene Inhibits Osteogenesis from Adipose-Derived Mesenchymal Stem Cells by Inducing Th17 Cell Differentiation

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