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Review

Interplay between Cytokine Circuitry and Transcriptional Regulation Shaping Helper T Cell Pathogenicity and Plasticity in Inflammatory Bowel Disease

by
Shin-Huei Fu
1,2,
Ming-Wei Chien
1,2,
Chao-Yuan Hsu
1,2,
Yu-Wen Liu
3,4 and
Huey-Kang Sytwu
1,2,*
1
National Institute of Infectious Disease and Vaccinology, National Health Research Institutes, No. 35, Keyan Road, Zhunan Town, Miaoli County 35053, Taiwan
2
Department and Graduate Institute of Microbiology and Immunology, National Defense Medical Center, No. 161, Section 6, Minquan East Road, Neihu District, Taipei 11490, Taiwan
3
Molecular Cell Biology, Taiwan International Graduate Program, Academia Sinica, No. 128, Academia Road, Section 2, Nankang, Taipei 11529, Taiwan
4
Graduate Institute of Life Sciences, National Defense Medical Center, No. 161, Section 6, Minquan East Road, Neihu District, Taipei 11490, Taiwan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(9), 3379; https://doi.org/10.3390/ijms21093379
Submission received: 15 April 2020 / Revised: 7 May 2020 / Accepted: 9 May 2020 / Published: 11 May 2020
(This article belongs to the Special Issue Pathophysiology in Colonic Diseases)
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Abstract

Inflammatory bowel disease (IBD) is a chronic disorder manifested as Crohn’s disease (CD) and ulcerative colitis (UC) characterized by intestinal inflammation and involves a dysregulated immune response against commensal microbiota through the activation of CD4 T helper cells. T helper cell differentiation to effector or regulatory phenotypes is controlled by cytokine networks and transcriptional regulators. Distinct polarized T helper cells are able to alter their phenotypes to adapt to diverse and fluctuating physiological environments. T helper cells exhibit intrinsic instability and flexibility to express cytokines of other lineages or transdifferentiate from one T helper cell type to another in response to various perturbations from physiological cytokine milieu as a means of promoting local immunity in response to injury or ensure tissue homeostasis. Furthermore, functional plasticity and diversity of T helper cells are associated with pathogenicity and are critical for immune homeostasis and prevention of autoimmunity. In this review, we provide deeper insights into the combinatorial extrinsic and intrinsic signals that control plasticity and transdifferentiation of T helper cells and also highlight the potential of exploiting the genetic reprogramming plasticity of T helper cells in the treatment of IBD.
Keywords: T helper cells; cytokines; transcription factors; plasticity; transdifferentiation; conversion; inflammatory bowel diseases; Crohn’s disease; ulcerative colitis T helper cells; cytokines; transcription factors; plasticity; transdifferentiation; conversion; inflammatory bowel diseases; Crohn’s disease; ulcerative colitis
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MDPI and ACS Style

Fu, S.-H.; Chien, M.-W.; Hsu, C.-Y.; Liu, Y.-W.; Sytwu, H.-K. Interplay between Cytokine Circuitry and Transcriptional Regulation Shaping Helper T Cell Pathogenicity and Plasticity in Inflammatory Bowel Disease. Int. J. Mol. Sci. 2020, 21, 3379. https://doi.org/10.3390/ijms21093379

AMA Style

Fu S-H, Chien M-W, Hsu C-Y, Liu Y-W, Sytwu H-K. Interplay between Cytokine Circuitry and Transcriptional Regulation Shaping Helper T Cell Pathogenicity and Plasticity in Inflammatory Bowel Disease. International Journal of Molecular Sciences. 2020; 21(9):3379. https://doi.org/10.3390/ijms21093379

Chicago/Turabian Style

Fu, Shin-Huei, Ming-Wei Chien, Chao-Yuan Hsu, Yu-Wen Liu, and Huey-Kang Sytwu. 2020. "Interplay between Cytokine Circuitry and Transcriptional Regulation Shaping Helper T Cell Pathogenicity and Plasticity in Inflammatory Bowel Disease" International Journal of Molecular Sciences 21, no. 9: 3379. https://doi.org/10.3390/ijms21093379

APA Style

Fu, S.-H., Chien, M.-W., Hsu, C.-Y., Liu, Y.-W., & Sytwu, H.-K. (2020). Interplay between Cytokine Circuitry and Transcriptional Regulation Shaping Helper T Cell Pathogenicity and Plasticity in Inflammatory Bowel Disease. International Journal of Molecular Sciences, 21(9), 3379. https://doi.org/10.3390/ijms21093379

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