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Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases

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Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases. / Bunte, Kübra; Beikler, Thomas.

in: INT J MOL SCI, Jahrgang 20, Nr. 14, 10.07.2019.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung

Harvard

Bunte, K & Beikler, T 2019, 'Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases', INT J MOL SCI, Jg. 20, Nr. 14. https://doi.org/10.3390/ijms20143394

APA

Bunte, K., & Beikler, T. (2019). Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases. INT J MOL SCI, 20(14). https://doi.org/10.3390/ijms20143394

Vancouver

Bunte K, Beikler T. Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases. INT J MOL SCI. 2019 Jul 10;20(14). https://doi.org/10.3390/ijms20143394

Bibtex

@article{8bfaa8bef19f41f69a9f8731eb4b576c,
title = "Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases",
abstract = "Innate immunity represents the semi-specific first line of defense and provides the initial host response to tissue injury, trauma, and pathogens. Innate immunity activates the adaptive immunity, and both act highly regulated together to establish and maintain tissue homeostasis. Any dysregulation of this interaction can result in chronic inflammation and autoimmunity and is thought to be a major underlying cause in the initiation and progression of highly prevalent immune-mediated inflammatory diseases (IMIDs) such as psoriasis, rheumatoid arthritis, inflammatory bowel diseases among others, and periodontitis. Th1 and Th2 cells of the adaptive immune system are the major players in the pathogenesis of IMIDs. In addition, Th17 cells, their key cytokine IL-17, and IL-23 seem to play pivotal roles. This review aims to provide an overview of the current knowledge about the differentiation of Th17 cells and the role of the IL-17/IL-23 axis in the pathogenesis of IMIDs. Moreover, it aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL-17/IL-23 axis.",
keywords = "Animals, Autoimmune Diseases/complications, Autoimmunity, Cell Differentiation, Cytokines/metabolism, Disease Management, Disease Susceptibility/immunology, Humans, Immunomodulation, Inflammation Mediators/metabolism, Inflammation/immunology, Interleukin-17/metabolism, Interleukin-23/metabolism, Periodontitis/diagnosis, Signal Transduction, Th17 Cells/cytology",
author = "K{\"u}bra Bunte and Thomas Beikler",
year = "2019",
month = jul,
day = "10",
doi = "10.3390/ijms20143394",
language = "English",
volume = "20",
journal = "INT J MOL SCI",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "14",

}

RIS

TY - JOUR

T1 - Th17 Cells and the IL-23/IL-17 Axis in the Pathogenesis of Periodontitis and Immune-Mediated Inflammatory Diseases

AU - Bunte, Kübra

AU - Beikler, Thomas

PY - 2019/7/10

Y1 - 2019/7/10

N2 - Innate immunity represents the semi-specific first line of defense and provides the initial host response to tissue injury, trauma, and pathogens. Innate immunity activates the adaptive immunity, and both act highly regulated together to establish and maintain tissue homeostasis. Any dysregulation of this interaction can result in chronic inflammation and autoimmunity and is thought to be a major underlying cause in the initiation and progression of highly prevalent immune-mediated inflammatory diseases (IMIDs) such as psoriasis, rheumatoid arthritis, inflammatory bowel diseases among others, and periodontitis. Th1 and Th2 cells of the adaptive immune system are the major players in the pathogenesis of IMIDs. In addition, Th17 cells, their key cytokine IL-17, and IL-23 seem to play pivotal roles. This review aims to provide an overview of the current knowledge about the differentiation of Th17 cells and the role of the IL-17/IL-23 axis in the pathogenesis of IMIDs. Moreover, it aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL-17/IL-23 axis.

AB - Innate immunity represents the semi-specific first line of defense and provides the initial host response to tissue injury, trauma, and pathogens. Innate immunity activates the adaptive immunity, and both act highly regulated together to establish and maintain tissue homeostasis. Any dysregulation of this interaction can result in chronic inflammation and autoimmunity and is thought to be a major underlying cause in the initiation and progression of highly prevalent immune-mediated inflammatory diseases (IMIDs) such as psoriasis, rheumatoid arthritis, inflammatory bowel diseases among others, and periodontitis. Th1 and Th2 cells of the adaptive immune system are the major players in the pathogenesis of IMIDs. In addition, Th17 cells, their key cytokine IL-17, and IL-23 seem to play pivotal roles. This review aims to provide an overview of the current knowledge about the differentiation of Th17 cells and the role of the IL-17/IL-23 axis in the pathogenesis of IMIDs. Moreover, it aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL-17/IL-23 axis.

KW - Animals

KW - Autoimmune Diseases/complications

KW - Autoimmunity

KW - Cell Differentiation

KW - Cytokines/metabolism

KW - Disease Management

KW - Disease Susceptibility/immunology

KW - Humans

KW - Immunomodulation

KW - Inflammation Mediators/metabolism

KW - Inflammation/immunology

KW - Interleukin-17/metabolism

KW - Interleukin-23/metabolism

KW - Periodontitis/diagnosis

KW - Signal Transduction

KW - Th17 Cells/cytology

U2 - 10.3390/ijms20143394

DO - 10.3390/ijms20143394

M3 - SCORING: Review article

C2 - 31295952

VL - 20

JO - INT J MOL SCI

JF - INT J MOL SCI

SN - 1661-6596

IS - 14

ER -