The role of Th17 cells in inflammatory bowel disease and the research progress

Chen, Lu; Ruan, Guangcong; Cheng, Yi; Yi, Ailin; Chen, Dongfeng; Wei, Yanling

doi:10.3389/fimmu.2022.1055914

Cited by 43 publications

(28 citation statements)

References 145 publications

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“…Innate immunity and inflammation are induced by Th17 through the secretion of cytokines such as IL‐17, IL‐21, IL‐22, IL‐26, and TNF‐α. Notably, Th17 promotes the development of immune‐related pathological damage, particularly autoimmune diseases 39–41 . DCs and CD4 + and CD8 + T cells are inhibited by Treg cells during immunosuppression 42 .…”

Section: Crosstalk Between Dcs and T Cellsmentioning

confidence: 99%

“…Notably, Th17 promotes the development of immune-related pathological damage, particularly autoimmune diseases. [39][40][41] DCs and CD4 + and CD8 + T cells are inhibited by Treg cells during immunosuppression. 42 This is achieved through two main mechanisms: (1) Inhibiting the capability of APCs to activate T cells, primarily through the interactions between CTLA-4, lymphocyte activation gene-3) on Treg surfaces and CD80, CD86, and major histocompatibility complexes (MHCs) on DC surfaces, respectively.…”

Section: T Cells Are the Key To The Occurrence And Development Of Tum...mentioning

confidence: 99%

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The DC–T cell axis is an effective target for the treatment of non‐small cell lung cancer

Wang,

Zhang,

Cui

et al. 2023

Immunity Inflam & Disease

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The dendritic cell (DC)‐T cell axis is a bridge that connects innate and adaptive immunities. The initial immune response against tumors is mainly induced by mature antigen‐presenting DCs. Enhancing the crosstalk between DCs and T cells may be an effective approach to improve the immune response to non‐small cell lung cancer (NSCLC). In this article, a review was made of the interaction between DCs and T cells in the treatment of NSCLC and how this interaction affects the treatment outcome.

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Section: Crosstalk Between Dcs and T Cellsmentioning

confidence: 99%

Section: T Cells Are the Key To The Occurrence And Development Of Tum...mentioning

confidence: 99%

The DC–T cell axis is an effective target for the treatment of non‐small cell lung cancer

Wang,

Zhang,

Cui

et al. 2023

Immunity Inflam & Disease

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“…The 3-, 7-and 12-oxo-bile acids, generated by the intestinal microbiota, have recently attracted attention because their potential to function as Retinoic Acid Receptor-Related Orphan Receptor (ROR)γt inverse agonists. RORγt is highly represented in Th17 and innate lymphoid cells (ILC)-3 and represent a well-defined therapeutic target in IBD 1, 15,[19][20][21][22][23] . In T cells, RORγt agonism promotes the differentiation from naive T cells toward Th17 cells whose activation promotes IBD development in human 24 .…”

Section: Introductionmentioning

confidence: 99%

A microbial derived bile acid acts as GPBAR1 agonist and RORγt inverse agonist and reverses inflammation in inflammatory bowel disease

Biagioli,

Di Giorgio,

Massa

et al. 2024

Preprint

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The interplay between the dysbiotic microbiota and bile acids is a critical determinant for development of a dysregulated immune system in inflammatory bowel disease (IBD). Here we have investigated the fecal bile acid metabolome, gut microbiota composition, and immune responses in IBD patients and murine models of colitis and found that IBD associates with an elevated excretion of primary bile acids while secondary, allo- and oxo- bile acids were reduced in both human and mice models of IBD. These changes correlated with the disease severity, mucosal expression of pro-inflammatory cytokines and chemokines, and reduced inflow of anti-inflammatory macrophages and Treg in the gut. Analysis of bile acids metabolome in the feces allowed the identification of five bile acids: 3-oxo-DCA, 3-oxo-LCA, allo-LCA, iso-allo-LCA and 3-oxo-UDCA, whose excretion was selectively decreased in IBD patients and diseased mice. By transactivation assay and docking calculations all five bile acids were shown to act as GPBAR1 agonists and RORγt inverse agonists, skewing Th17/Treg ratio and macrophage polarization toward an M2 phenotype. In a murine model of colitis, administration of 3-oxo-DCA suffices to reverse colitis development and intestinal dysbiosis in a GPBAR1-dependent manner.In vivoadministration of 3-oxo-DCA to colitic mice also reserves disease severity and RORγt activation induced by a RORγt agonist and IL-23, a Th17 inducing cytokine. These results demonstrated intestinal excretion of 3-oxoDCA, a dual GPBAR1 agonist and RORγt inverse agonist, is reduced in IBD and models of colitis and its restitution protects against colitis development, highlighting a potential role for this agent in IBD management.

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“…Th17 cells, together with regulatory T cells (Tregs), are in dynamic balance and cooperate in maintaining the homeostasis of the immune microenvironment and gut health. Specifically, Th17 cells, under the condition of homeostasis, secrete small amounts of IL-17 and IL-22 by promoting epithelial cell proliferation and upregulating the expression of antimicrobial peptides and tight junction proteins, thus protecting the intestinal mucosa from external insults [ 50 ]. When the diversity and composition of the gut microbiota are disrupted because of environmental factors or the regulation of susceptibility genes, pathogenic bacteria can promote colonization and infection by breaking down mucin-like nutrients, releasing toxic gases, and secreting enzymes to destroy mucosal barriers.…”

Section: Introductionmentioning

confidence: 99%

“…When the diversity and composition of the gut microbiota are disrupted because of environmental factors or the regulation of susceptibility genes, pathogenic bacteria can promote colonization and infection by breaking down mucin-like nutrients, releasing toxic gases, and secreting enzymes to destroy mucosal barriers. In these cases, there is an increase in the number of Th17 cells with IL-17 expression in the foci of inflammation [ 50 ].…”

Section: Introductionmentioning

confidence: 99%

Dietary Polyphenols, Microbiome, and Multiple Sclerosis: From Molecular Anti-Inflammatory and Neuroprotective Mechanisms to Clinical Evidence

Rosa

Lonardo

Cacciapuoti

et al. 2023

IJMS

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Multiple sclerosis (MS) is a multifactorial, immune-mediated disease caused by complex gene-environment interactions. Dietary factors modulating the inflammatory status through the control of the metabolic and inflammatory pathways and the composition of commensal gut microbiota, are among the main environmental factors involved in the pathogenesis of MS. There is no etiological therapy for MS and the drugs currently used, often accompanied by major side effects, are represented by immunomodulatory substances capable of modifying the course of the disease. For this reason, nowadays, more attention is paid to alternative therapies with natural substances with anti-inflammatory and antioxidant effects, as adjuvants of classical therapies. Among natural substances with beneficial effects on human health, polyphenols are assuming an increasing interest due to their powerful antioxidant, anti-inflammatory, and neuroprotective effects. Beneficial properties of polyphenols on the CNS are achieved through direct effects depending on their ability to cross the blood-brain barrier and indirect effects exerted in part via interaction with the microbiota. The aim of this review is to examine the literature about the molecular mechanism underlying the protective effects of polyphenols in MS achieved by experiments conducted in vitro and in animal models of the disease. Significant data have been accumulated for resveratrol, curcumin, luteolin, quercetin, and hydroxytyrosol, and therefore we will focus on the results obtained with these polyphenols. Clinical evidence for the use of polyphenols as adjuvant therapy in MS is restricted to a smaller number of substances, mainly curcumin and epigallocatechin gallate. In the last part of the review, a clinical trial studying the effects of these polyphenols in MS patients will also be revised.

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The role of Th17 cells in inflammatory bowel disease and the research progress

Cited by 43 publications

References 145 publications

The DC–T cell axis is an effective target for the treatment of non‐small cell lung cancer

The DC–T cell axis is an effective target for the treatment of non‐small cell lung cancer

A microbial derived bile acid acts as GPBAR1 agonist and RORγt inverse agonist and reverses inflammation in inflammatory bowel disease

Dietary Polyphenols, Microbiome, and Multiple Sclerosis: From Molecular Anti-Inflammatory and Neuroprotective Mechanisms to Clinical Evidence

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