中国P站

Oral tolerance; Regulatory T cells; Tregs; Mucosal immunity; Cytokines; Dendritic cells; Oral microbiome; Inflammation; Tolerance induction; Genetic factors

Introduction

Oral tolerance induction depends on regulatory T cells (Tregs) in the oral mucosa, which prevent chronic inflammation by suppressing immune responses to harmless antigens [1].

Disruption of this balance can cause inflammatory bowel disease. Epithelial cells are key in modulating mucosal immunity by producing cytokines and chemokines that affect the differentiation and activity of immune cells, including Tregs, in the oral mucosa [2].

The oral microbiome has a significant impact on mucosal immunity, and dysbiosis can disrupt the balance of pro- and anti-inflammatory responses, thereby affecting Treg development and function [3].

Specific cytokines like TGF-β and IL-10 are critical for Treg induction and maintenance in the oral mucosa, promoting suppressive functions and dampening inflammatory responses [4].

Dendritic cells (DCs) are crucial for presenting antigens to T cells and influencing their differentiation; tolerogenic DCs in the oral mucosa promote Treg development, contributing to oral tolerance [5].

Genetic factors influence susceptibility to oral inflammatory diseases, with variations in genes involved in immune regulation affecting Treg function and oral tolerance [6].

The oral mucosa is constantly exposed to antigens from food, commensal bacteria, and pathogens, requiring the immune system to differentiate between harmless and harmful antigens to maintain oral tolerance [7].

Environmental factors like diet and pollutants can influence oral mucosal immunity and Treg function, potentially disrupting oral tolerance and contributing to inflammatory diseases [8].

Therapeutic strategies targeting Tregs to enhance oral tolerance are under active research, aiming to prevent or treat oral inflammatory diseases [9].

Understanding the mechanisms of oral mucosal immunity, tolerance induction, and Treg biology is essential for developing effective strategies to prevent and treat oral inflammatory diseases [10].

Description

Oral tolerance hinges on the functionality of regulatory T cells (Tregs) within the oral mucosa. These Tregs are responsible for suppressing immune responses to harmless antigens, effectively preventing chronic inflammation. Imbalances in this system can lead to conditions like inflammatory bowel disease [1]. Epithelial cells contribute significantly to mucosal immunity. They release cytokines and chemokines, influencing the behavior and differentiation of immune cells, especially Tregs, within the oral mucosa [2].

The oral microbiome's state has substantial effects on mucosal immunity. When dysbiosis occurs, the balance between pro- and anti-inflammatory responses is disrupted. This disruption affects both the development and function of Tregs [3]. Certain cytokines, notably TGF-β and IL-10, are indispensable for inducing and maintaining Tregs in the oral mucosa. They facilitate the suppressive actions of Tregs, thereby mitigating inflammatory responses [4].

Dendritic cells (DCs) are vital in antigen presentation to T cells, directing their differentiation pathways. In the oral mucosa, tolerogenic DCs encourage the growth of Tregs, reinforcing oral tolerance [5]. Genetic factors also play a role in the risk of developing oral inflammatory diseases. Variations in immune regulation genes can influence Treg function, impacting oral tolerance [6].

Because the oral mucosa is continuously exposed to antigens from various sources—food, commensal bacteria, and pathogens—the immune system must distinguish between threats and non-threats to maintain oral tolerance [7]. Environmental elements, including diet and pollutants, can shift oral mucosal immunity and Treg function. These environmental factors can disturb oral tolerance, potentially leading to inflammatory diseases [8]. Therapeutic strategies aimed at Tregs to improve oral tolerance are actively being explored, with the goal of preventing or treating oral inflammatory diseases [9]. A thorough understanding of oral mucosal immunity, tolerance induction, and Treg biology is key to creating effective prevention and treatment plans for oral inflammatory diseases [10].

Conclusion

Oral tolerance induction depends on the presence and function of regulatory T cells (Tregs) within the oral mucosa, which suppress immune responses to harmless antigens, preventing chronic inflammation. The disruption of this delicate balance can lead to inflammatory conditions. Epithelial cells play a crucial role in modulating mucosal immunity by producing cytokines and chemokines that influence the differentiation and activity of immune cells, including Tregs. The oral microbiome significantly impacts mucosal immunity; dysbiosis can disrupt the balance of pro- and anti-inflammatory responses, affecting Treg development and function. Specific cytokines, like TGF-β and IL-10, are critical for Treg induction and maintenance in the oral mucosa, promoting suppressive functions and dampening inflammatory responses. Dendritic cells (DCs) are also key players, presenting antigens to T cells and influencing their differentiation. Tolerogenic DCs promote Treg development, contributing to oral tolerance. Genetic factors influence the susceptibility to oral inflammatory diseases, with variations in immune regulation genes affecting Treg function and oral tolerance. Environmental factors like diet and pollutants can influence oral mucosal immunity and Treg function, potentially disrupting oral tolerance and contributing to inflammatory diseases. Therapeutic strategies targeting Tregs to enhance oral tolerance are under active research, aiming to prevent or treat oral inflammatory diseases. Understanding the mechanisms of oral mucosal immunity, tolerance induction, and Treg biology is essential for developing effective strategies to prevent and treat oral inflammatory diseases.

References

1. Elizabeth RM, Neil M, Soha R (2016) .Mucosal Immunol 9:171-183.

   , ,

2. Annika L, Berit TB, Emma AB (2019) .Mucosal Immunol 12:1219-1231.

   , ,

3. Sophie PR, Chiara V, Markus BG (2019) .Cell Host Microbe 25:509-521.e504.

   , ,

4. Mark OL, Yi-Yan W, Sanjabi S (2006) .Annu Rev Immunol 24:99-146.

   , ,

5. Ali W, Nicolas F, Virginie B (2003) .Immunity 18:289-301.

   , ,

6. Jost WG, Marianne KV, Eirik F (2016) .J Autoimmun 74:1-16.

   , ,

7. Per B, Gunnar H, Jorunn R (1996) .Gut 39:333-343.

   , ,

8. Yoshinori F, Marzieh TS, Tonse NKR (2016) .J Allergy Clin Immunol 138:1271-1278.

   , ,

9. Shimon S, Takahiro Y, Takayuki N (2008) .Cell 133:775-787.

   , ,

10. Yasmine B, Trevor WH (2014) .Cell 157:121-141.

    , ,