An emphasis of T cell subsets as regulators of periodontal health and disease

Balaji, Saranya; Cholan, Priyanka K; Victor, Dhayanand John

doi:10.18053/jctres.07.202105.002

Cited by 9 publications

(7 citation statements)

References 66 publications

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“…CD8 + cytotoxic T-lymphocytes (CTL) release vesicles containing perforin and granzyme, inducing death of target cells. CD8 + T-regs reduce osteoclastogenesis by producing IL-10 and TGF-β ( 139 ).…”

Section: Periodontal Diseasementioning

confidence: 99%

“…The production of opsonizing antibodies makes the targeting of microbes by phagocytic cells more efficient. B-regs are a B-cell subset, producing IL-10, IL-35, and TGF-β1 to reduce inflammation and inhibit bone resorption ( 139 , 141 ). Mice with B-cell deficiency have increased ligature induced periodontal bone loss compared to wild -type mice, suggesting that B-cells may be protective ( 142 ).…”

Section: Periodontal Diseasementioning

confidence: 99%

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Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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Periodontitis involves the loss of connective tissue attachment and alveolar bone. Single cell RNA-seq experiments have provided new insight into how resident cells and infiltrating immune cells function in response to bacterial challenge in periodontal tissues. Periodontal disease is induced by a combined innate and adaptive immune response to bacterial dysbiosis that is initiated by resident cells including epithelial cells and fibroblasts, which recruit immune cells. Chemokines and cytokines stimulate recruitment of osteoclast precursors and osteoclastogenesis in response to TNF, IL-1β, IL-6, IL-17, RANKL and other factors. Inflammation also suppresses coupled bone formation to limit repair of osteolytic lesions. Bone lining cells, osteocytes and periodontal ligament cells play a key role in both processes. The periodontal ligament contains cells that exhibit similarities to tendon cells, osteoblast-lineage cells and mesenchymal stem cells. Bone lining cells consisting of mesenchymal stem cells, osteoprogenitors and osteoblasts are influenced by osteocytes and stimulate formation of osteoclast precursors through MCSF and RANKL, which directly induce osteoclastogenesis. Following bone resorption, factors are released from resorbed bone matrix and by osteoclasts and osteal macrophages that recruit osteoblast precursors to the resorbed bone surface. Osteoblast differentiation and coupled bone formation are regulated by multiple signaling pathways including Wnt, Notch, FGF, IGF-1, BMP, and Hedgehog pathways. Diabetes, cigarette smoking and aging enhance the pathologic processes to increase bone resorption and inhibit coupled bone formation to accelerate bone loss. Other bone pathologies such as rheumatoid arthritis, post-menopausal osteoporosis and bone unloading/disuse also affect osteoblast lineage cells and participate in formation of osteolytic lesions by promoting bone resorption and inhibiting coupled bone formation. Thus, periodontitis involves the activation of an inflammatory response that involves a large number of cells to stimulate bone resorption and limit osseous repair processes.

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Section: Periodontal Diseasementioning

confidence: 99%

Section: Periodontal Diseasementioning

confidence: 99%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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“…Furthermore, we investigated the secretion of functional cytokines (IFN-γ, IL-17A, IL-4, IL-10 and TGF-β) by CD4 + T lymphocytes. IFN-γ is mainly produced by Th1 lymphocytes ( 46 ), IL-17A is characteristically secreted by Th17 lymphocytes ( 47 ), and IL-10 and TGF-β are expressed by Tregs ( 48 ). All three CD4 + T lymphocyte subsets play essential roles during periodontitis pathogenesis ( 46 ).…”

Section: Discussionmentioning

confidence: 99%

“…IFN-γ is mainly produced by Th1 lymphocytes ( 46 ), IL-17A is characteristically secreted by Th17 lymphocytes ( 47 ), and IL-10 and TGF-β are expressed by Tregs ( 48 ). All three CD4 + T lymphocyte subsets play essential roles during periodontitis pathogenesis ( 46 ). IL-4, a distinctive cytokine for Th2 lymphocytes, was not detectable.…”

Section: Discussionmentioning

confidence: 99%

25-hydroxyvitamin D3 generates immunomodulatory plasticity in human periodontal ligament-derived mesenchymal stromal cells that is inflammatory context-dependent

et al. 2023

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IntroductionHuman periodontal ligament-derived mesenchymal stromal cells (hPDL-MSCs) exhibit a tight bi-directional interaction with CD4+ T lymphocytes. The hPDL-MSCs’ immunomodulatory abilities are drastically enhanced by pro-inflammatory cytokines via boosting the expression of various immunomediators. 25-hydroxyvitamin D3 (25(OH)D3), the major metabolite of vitamin D3 in the blood, affects both hPDL-MSCs and CD4+ T lymphocytes, but its influence on their interaction is unknown.MethodsTherefore, primary hPDL-MSCs were stimulated in vitro with tumor necrosis factor (TNF)-α a or interleukin (IL)-1β in the absence and presence of 25(OH)D3 followed by an indirect co-culture with phytohemagglutinin-activated CD4+ T lymphocytes. The CD4+ T lymphocyte proliferation, viability, and cytokine secretion were analyzed. Additionally, the expression of various immunomediators in hPDL-MSCs was investigated, and their implication was verified by using pharmacological inhibitors.Results25(OH)D3 significantly counteracted the suppressive effects of IL-1β-treated hPDL-MSCs on CD4+ T lymphocyte proliferation, whereas no effects were observed in the presence of TNF-α. Additionally, 25(OH)D3 significantly increased the percentage of viable CD4+ T lymphocytes via TNF-α- or IL-1β-treated hPDL-MSCs. It also caused a significant decrease in interferon-γ, IL-17A, and transforming growth factor-β productions, which were triggered by TNF-α-treated hPDL-MSCs. 25(OH)D3 significantly decreased the production of various immunomediators in hPDL-MSCs. Inhibition of two of them, prostaglandin E2 and indoleamine-2,3-dioxygenase-1, partially abolished some of the hPDL-MSCs-mediated effects of 25(OH)D3 on CD4+ T lymphocytes.ConclusionThese data indicate that 25(OH)D3 influences the immunomodulatory activities of hPDL-MSCs. This modulatory potential seems to have high plasticity depending on the local cytokine conditions and may be involved in regulating periodontal tissue inflammatory processes.

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“…CD8+ T-cells are fewer in number than CD4+ T-cells in periodontitis lesions ( 84 ). CD8+ cytotoxic T lymphocytes produce TNF, IFN-γ and kill cells through expression of Fas ligands, pore-forming proteins (perforins) and proteases (granzyme) ( 85 ). CD8+ regulatory T lymphocytes (CD8+ Tregs) produce CTLA4, TGF-b and IL-10 to resolve inflammation.…”

Section: Adaptive Immunitymentioning

confidence: 99%

An update on periodontal inflammation and bone loss

Zhang,

Liu,

Afzali

et al. 2024

Front. Immunol.

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Periodontal disease is a chronic inflammatory condition that affects the supporting structures of the teeth, including the periodontal ligament and alveolar bone. Periodontal disease is due to an immune response that stimulates gingivitis and periodontitis, and its systemic consequences. This immune response is triggered by bacteria and may be modulated by environmental conditions such as smoking or systemic disease. Recent advances in single cell RNA-seq (scRNA-seq) and in vivo animal studies have provided new insight into the immune response triggered by bacteria that causes periodontitis and gingivitis. Dysbiosis, which constitutes a change in the bacterial composition of the microbiome, is a key factor in the initiation and progression of periodontitis. The host immune response to dysbiosis involves the activation of various cell types, including keratinocytes, stromal cells, neutrophils, monocytes/macrophages, dendritic cells and several lymphocyte subsets, which release pro-inflammatory cytokines and chemokines. Periodontal disease has been implicated in contributing to the pathogenesis of several systemic conditions, including diabetes, rheumatoid arthritis, cardiovascular disease and Alzheimer’s disease. Understanding the complex interplay between the oral microbiome and the host immune response is critical for the development of new therapeutic strategies for the prevention and treatment of periodontitis and its systemic consequences.

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An emphasis of T cell subsets as regulators of periodontal health and disease

Cited by 9 publications

References 66 publications

Impact of the host response and osteoblast lineage cells on periodontal disease

Impact of the host response and osteoblast lineage cells on periodontal disease

25-hydroxyvitamin D3 generates immunomodulatory plasticity in human periodontal ligament-derived mesenchymal stromal cells that is inflammatory context-dependent

An update on periodontal inflammation and bone loss

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