T-helper 22 cells develop as a distinct lineage from Th17 cells during bacterial infection and phenotypic stability is regulated by T-bet

Barnes, Jessica; Plank, Maximilian; Asquith, Kelly L.; Maltby, Steven; Sabino, Lorena R; Kaiko, Gerard E.; Lochrin, Alyssa J.; Horvat, Jay C.; Mayall, Jemma; Kim, Richard; Hansbro, Philip M.; Keely, Simon; Belz, Gabrielle T.; Tay, Hock L.; Foster, Paul S.

doi:10.1038/s41385-021-00414-6

Cited by 13 publications

(14 citation statements)

References 51 publications

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“…Additionally, Th22 cells remain stable under inducible Th1, Th2, Th17, and Treg cells conditions, which reinforced that Th22 cells are a novel effector T subtype contributing to skin homeostasis and inflammation ( 10 ). Furthermore, results from an IL-17A fate-mapping reporter assay and a transcription profile supported Th22 cells as a distinct lineage from Th17 cells ( 12 , 13 ).…”

Section: Introductionmentioning

confidence: 89%

“…Recently, Foster's team generated IL17aeGFPIL22tdTom dual-reporter transgenic mice and proved that Th22 cells were not derived from Th17 cells as a distinct lineage in Th22-enriched culture conditions (12). Further, they validated this finding in vivo with triple-reporter mice in which Th22 cells seldom developed through the IL-17Aexpressing stage during bacterial infection (13). Collectively, Th22 cells are regarded as a novel T cell subset.…”

Section: Characterization and Differentiation Of Th22 Cellsmentioning

confidence: 99%

“…Plasticity allows for heterogeneity, which facilitates Th cells to continuously adapt to the ever-changing surroundings and is crucial for immune homeostasis ( 31 , 51 ). Studies have demonstrated that a proportion of Th22 cells can express IFN-γ ( 10 , 12 , 28 , 32 ), IL-4 ( 10 ) IL-13 ( 12 , 28 ), and IL-17 ( 10 , 12 , 13 , 32 ), indicating a possible conversion from Th22 cells to Th1/2/17 cells. In turn, Th17 clones, derived from psoriatic skin, could be polarized to an IL-22-single-producing Th22 cell profile ( 52 ).…”

Section: Characterization and Differentiation Of Th22 Cellsmentioning

confidence: 99%

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The Role of T Helper 22 Cells in Dermatological Disorders

Pan

Wang

et al. 2022

Front. Immunol.

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T helper 22 (Th22) cells are a newly identified subset of CD4+ T cells that secrete the effector cytokine interleukin 22 (IL-22) upon specific antigen stimulation, barely with IFN-γ or IL-17. Increasing studies have demonstrated that Th22 cells and IL-22 play essential roles in skin barrier defense and skin disease pathogenesis since the IL-22 receptor is widely expressed in the skin, especially in keratinocytes. Herein, we reviewed the characterization, differentiation, and biological activities of Th22 cells and elucidated their roles in skin health and disease. We mainly focused on the intricate crosstalk between Th22 cells and keratinocytes and provided potential therapeutic strategies targeting the Th22/IL-22 signaling pathway.

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Section: Introductionmentioning

confidence: 89%

Section: Characterization and Differentiation Of Th22 Cellsmentioning

confidence: 99%

Section: Characterization and Differentiation Of Th22 Cellsmentioning

confidence: 99%

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The Role of T Helper 22 Cells in Dermatological Disorders

Pan

Wang

et al. 2022

Front. Immunol.

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“…109 Although commitment from naive CD4 T cells into Th22 depends on exposure to IL-6, IL-1β, and IL-23 and absence of TGFβ (Figure 1), Th22 molecular switches have not been identified yet, with equivocal reports on the respective role of RORγt and Tbet in this process. [109][110][111] Th22 cells secrete IL-22, IL-13, and TNFα, and are characterized by the expression of chemokine receptors CCR4, CCR6, and CCR10. 109,112 Depending on the context, Th22 cells can gain Th1-like or Th2-like properties but do not produce IL-17.…”

Section: Th22 Cellsmentioning

confidence: 99%

Neuroinflammation: Extinguishing a blaze of T cells

Benallegue

Kébir

Alvarez

2022

Immunological Reviews

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Summary Inflammation is a biological process that dynamically alters the surrounding microenvironment, including participating immune cells. As a well‐protected organ surrounded by specialized barriers and with immune privilege properties, the central nervous system (CNS) tightly regulates immune responses. Yet in neuroinflammatory conditions, pathogenic immunity can disrupt CNS structure and function. T cells in particular play a key role in promoting and restricting neuroinflammatory responses, while the inflamed CNS microenvironment can influence and reshape T cell function and identity. Still, the contraction of aberrant T cell responses within the CNS is not well understood. Using autoimmunity as a model, here we address the contribution of CD4 T helper (Th) cell subsets in promoting neuropathology and disease. To address the mechanisms antagonizing neuroinflammation, we focus on the control of the immune response by regulatory T cells (Tregs) and describe the counteracting processes that preserve their identity under inflammatory challenges. Finally, given the influence of the local microenvironment on immune regulation, we address how CNS‐intrinsic signals reshape T cell function to mitigate abnormal immune T cell responses.

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“…Th22 and Th9 cells have been identified as new Th cells subsets which are phenotypically distinct from other Th cells ( 107 , 108 ). Th22 cells mainly secrete IL-22 which is also produced by Th17 cells, but Th22 cells hardly produce IL-17 ( 109 ).…”

Section: The Function Of Cd4 + T Cells In Periodon...mentioning

confidence: 99%

mTOR Signaling in the Regulation of CD4+ T Cell Subsets in Periodontal Diseases

Jiang

Huang

et al. 2022

Front. Immunol.

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Periodontal disease results from the inflammatory infiltration by the microbial community which is marked through tooth mobility and alveolar bone resorption. The inflammation in periodontal disease is mediated by CD4+ T cells through cytokine secretion and osteoclastogenetic activity. Historically, the inflammatory model in periodontal disease is described through disruption of the balance between two subsets of T helper cells which are T-helper type 1 (Th1) and T-helper type 2 (Th2). However, more and more studies have found that apart from subsets of helper T cells, regulatory T-cells and Th17 cells are also involved in the pathogenesis of periodontal diseases. Growing evidence proves that helper T cells differentiation, activation, and subset determination are under the strong impact of mTOR signaling. mTOR signaling could promote Th1 and Th17 cell differentiation and inhibit Treg commitment through different mTOR complexes, therefore we anticipate a regulation effect of mTOR signaling on periodontal diseases by regulating CD4+ T cell subsets. This review aims to integrate the topical researches about the role of different types of Th cells in the pathogenesis of periodontal diseases, as well as the regulation of mTOR signaling in the specification and selection of Th cell commitment.

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T-helper 22 cells develop as a distinct lineage from Th17 cells during bacterial infection and phenotypic stability is regulated by T-bet

Cited by 13 publications

References 51 publications

The Role of T Helper 22 Cells in Dermatological Disorders

The Role of T Helper 22 Cells in Dermatological Disorders

Neuroinflammation: Extinguishing a blaze of T cells

mTOR Signaling in the Regulation of CD4+ T Cell Subsets in Periodontal Diseases

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