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

Naufel, André Oliveira; Aguiar, Maria Cássia Ferreira de; Madeira, Fernandes Moreira; Abreu, Lucas Guimarães

doi:10.1590/1807-3107bor-2017.vol31.0103

Cited by 21 publications

(18 citation statements)

References 36 publications

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“…It is worth noting that in contrast to the present study, progressive effort on the mechanical treadmill did not trigger changes in Th17 cell percentage. The increase in IL-6 plasma level is one of the most probable promoters of Th17 cell differentiation [12,60]. This observation helps to explain our findings of a post-effort increase in Th17 cell percentage without an increase in IL-17A levels.…”

Section: Post-effort Cytokine Releasesupporting

confidence: 61%

“…Physical effort induces significant disorders of homeostasis on a physiological, immunological and molecular level [1][2][3][4][5][6][7][8]. Although the role of peripheral leukocytes is widely discussed in the literature [9][10][11][12][13][14][15][16], the regulatory mechanisms affecting the modulation of the immune system, especially T cells, which accompany the progressive effort to exhaustion are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

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T helper cell-related changes in peripheral blood induced by progressive effort among soccer players

Kostrzewa-Nowak

Nowak

2020

PLoS ONE

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The regulatory mechanisms affecting the modulation of the immune system accompanying the progressive effort to exhaustion, particularly associated with T cells, are not fully understood. We analysed the impact of two progressive effort protocols on T helper (Th) cell distribution and selected cytokines. Methods Sixty-two male soccer players with a median age of 17 (16-29) years performed different protocols for progressive exercise until exhaustion: YO-YO (YYRL1) and Beep. Blood samples for all analyses were taken three times: at baseline, post-effort, and in recovery. Results The percentage of Th1 cells increased post-effort and in recovery. The post-effort percentage of Th1 cells was higher in the Beep group compared to the YYRL1 group. Significant post-effort increase in Th17 cells was observed in both groups. The post-effort percentage of regulatory T cells (Treg) increased in the Beep group. An increased post-effort concentration of IL-2, IL-6, IL-8 and IFN-γ in both groups was observed. Post-effort TNF-α and IL-10 levels were higher than baseline in the YYRL1 group, while the post-effort IL-17A concentration was lower than baseline only in the Beep group. The recovery IL-2, IL-4, TNF-α and IFN-γ levels were higher than baseline in the YYRL1 group. The recovery IL-4, IL-6, IL-8, TNF-α and IFN-γ values were higher than baseline in the Beep group. Conclusion The molecular patterns related to cytokine secretion are not the same between different protocols for progressive effort. It seems that Treg cells are probably the key cells responsible for silencing the inflammation and enhancing anti-inflammatory pathways.

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Section: Post-effort Cytokine Releasesupporting

confidence: 61%

Section: Introductionmentioning

confidence: 99%

T helper cell-related changes in peripheral blood induced by progressive effort among soccer players

Kostrzewa-Nowak

Nowak

2020

PLoS ONE

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“…Discrepant results were found in studies aimed at detecting these cells in periapical cysts and granulomas. This fact may be attributed to the apoptosis process the dendritic cells undergo after presentation of an antigen, tissue repair process characterised by lower number of these cells, maturation profile of these cells and difference in the methods used by authors [42][43][44].…”

Section: Inflammatory Cellsmentioning

confidence: 99%

“…These cytokines have opposite effects, but with no mutual inhibition. While TGF-b is a potent immune-modulating cytokine, IL-17 is capable to reactivate the inflammatory process by stimulating the production of IL-8 [38,43], meaning that re-acutisation of chronic apical periodontitis is closely related to higher levels of IL-17 and increased infiltration of leukocytes [12,13].…”

Section: Cytokinesmentioning

confidence: 99%

Inflammatory profile of chronic apical periodontitis: a literature review

Braz‐Silva

Bergamini

Mardegan

et al. 2018

Acta Odontologica Scandinavica

123

100

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Apical periodontitis caused by root canal infection is the most frequent pathological lesion in the jaws, mainly manifested as periapical granulomas and cysts. Understanding of the formation and progression of apical periodontitis as well as the identification of inflammatory biomarkers can help increase the knowledge of pathogenic mechanisms, improve the diagnosis and provide support for different therapeutic strategies. The objective of the present article is to review inflammatory biomarkers such as cytokines, chemokines, inflammatory cells, neuropeptides, RANK/RANKL/OPG system and other inflammatory markers and to relate these systems to the development and progression of pathological conditions related to apical periodontitis.

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“…Helper T lymphocytes also exhibit various subtypes, such as T helper type 1 (Th1), Th2, Th17, and regulatory T cells. All helper T lymphocyte subtypes are associated with various inflammatory diseases . In particular, the balance between Th1 and Th2 lymphocytes, and pro‐inflammatory M1 and anti‐inflammatory M2 macrophages determines the macrophage subtype‐based inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory response under zinc deficiency is exacerbated by dysfunction of the T helper type 2 lymphocyte–M2 macrophage pathway

et al. 2019

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Nutritional zinc deficiency leads to immune dysfunction and aggravates inflammation. However, the underlying mechanism remains unknown. In this study, the relationship between macrophage subtypes (M1 and M2) and helper T lymphocytes (Th1 and Th2) was investigated using the spleen from rats fed zinc-deficient or standard diet. In experiment I, 5week-old male Sprague-Dawley rats were fed a zinc-deficient diet (without zinc additives) or a standard diet (containing 0Á01% zinc) for 6 weeks. In experiment II, the rats were divided into four groups: one group was fed a standard diet for 6 weeks; two groups were fed zinc-deficient diets and were injected three times a week with either saline or interleukin-4 (IL-4) (zinc-deficient/IL-4 i.p.); a fourth group (zinc-deficient/standard) was fed a zinc-deficient diet for 6 weeks followed by a standard diet for 4 weeks. In experiment I; GATA-binding protein 3 (GATA-3) protein level, M2 macrophage, CD3 + CD8 + cells, and IL-4/IL-13-positive cells significantly decreased in the spleens of the zinc-deficient group. Additionally, IL-1b and macrophage inflammatory protein-1a (MIP-1a) mRNA levels significantly increased in the splenic macrophages of the zinc-deficient group. In experiment II; M2 macrophages, CD3 + CD8 + cells, IL-4/IL-13-positive cells, and GATA-3 protein levels significantly increased in the spleens of the zinc-deficient/IL-4 i.p. and zinc-deficient/standard groups. Furthermore, IL-1b and MIP-1a mRNA levels decreased in the splenic macrophages of the zinc-deficient/IL-4 i.p. and zinc-deficient/standard groups. Zinc deficiency-induced aggravated inflammation is related to Th2 lymphocytes and followed by the association with loss of GATA-3, IL-4 and anti-inflammatory M2 macrophages. Importantly, IL-4 injection or zinc supplementation can reverse the effects of zinc deficiency on immune function.

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

Cited by 21 publications

References 36 publications

T helper cell-related changes in peripheral blood induced by progressive effort among soccer players

T helper cell-related changes in peripheral blood induced by progressive effort among soccer players

Inflammatory profile of chronic apical periodontitis: a literature review

Inflammatory response under zinc deficiency is exacerbated by dysfunction of the T helper type 2 lymphocyte–M2 macrophage pathway

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