Programmed cell death: immune regulatory mechanisms in periodontitis and rheumatoid arthritis.
4 affiliations
- 1The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangdong, China.
- 2Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Guangzhou/Foshan, China.
- 3Medical Center of Stomatology, The First Affiliated Hospital, Jinan University, Guangzhou, China.
- 4Zeren Dental Clinic (Guangzhou) Co., Ltd., Guangzhou, China.
Abstract
Periodontitis and rheumatoid arthritis, as chronic inflammatory diseases that share epidemiological associations and immunopathological characteristics, have various forms of programmed cell death (PCD) that play a core role in their pathogenesis, which form an important link between the two. The comorbidity of periodontitis and rheumatoid arthritis suggests that there might be a common immune regulatory mechanism, with PCD pathways playing a key role in regulating immune responses. Particularly, the Th17/Treg imbalance and apoptosis resistance in CD4⁺CD28⁻ T cells emerge as shared T cell-centered mechanisms bridging periodontal infection to rheumatoid autoimmunity. Studying how PCD works in periodontitis and rheumatoid arthritis can help uncover the potential links between the two diseases, which provides new targets for clinical treatment and improves patient prognosis. In this article, we'll review relevant research and discuss how PCD is important for immune regulation in periodontitis and rheumatoid arthritis, which provides a theoretical basis for future treatment strategies for both conditions, helping to control the progression of inflammation more effectively.
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BibTeX
@article{chan2026programmed,
title = {{Programmed cell death: immune regulatory mechanisms in periodontitis and rheumatoid arthritis.}},
author = {Hei Chan and XuFeng Chen and Jianwen Deng and Yuyan Mai},
journal = {Frontiers in cell and developmental biology},
year = {2026},
month = oct,
doi = {10.3389/fcell.2026.1815945},
url = {https://europepmc.org/article/MED/42936105},
note = {CC BY},
}
RIS
TY - JOUR
TI - Programmed cell death: immune regulatory mechanisms in periodontitis and rheumatoid arthritis.
AU - Hei Chan
AU - XuFeng Chen
AU - Jianwen Deng
AU - Yuyan Mai
PY - 2026
DA - 2026/10/12
JO - Frontiers in cell and developmental biology
DO - 10.3389/fcell.2026.1815945
UR - https://europepmc.org/article/MED/42936105
AB - Periodontitis and rheumatoid arthritis, as chronic inflammatory diseases that share epidemiological associations and immunopathological characteristics, have various forms of programmed cell death (PCD) that play a core role in their pathogenesis, which form an important link between the two. The comorbidity of periodontitis and rheumatoid arthritis suggests that there might be a common immune regulatory mechanism, with PCD pathways playing a key role in regulating immune responses. Particularly, the Th17/Treg imbalance and apoptosis resistance in CD4⁺CD28⁻ T cells emerge as shared T cell-centered mechanisms bridging periodontal infection to rheumatoid autoimmunity. Studying how PCD works in periodontitis and rheumatoid arthritis can help uncover the potential links between the two diseases, which provides new targets for clinical treatment and improves patient prognosis. In this article, we'll review relevant research and discuss how PCD is important for immune regulation in periodontitis and rheumatoid arthritis, which provides a theoretical basis for future treatment strategies for both conditions, helping to control the progression of inflammation more effectively.
SN - 2296-634X
ER -