Th1/Th2 Balance and Th17/Treg-Mediated Immunity in relation to Murine Resistance to Dextran Sulfate-Induced Colitis

Yang, Fang; Wang, Danan; Li, Yan; Sang, Li-Xuan; Zhu, Jü; Wang, Jinyan; Wei, Bing; Lu, Cuihua; Sun, Xun

doi:10.1155/2017/7047201

Cited by 49 publications

(44 citation statements)

References 43 publications

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“…Previous reports -including results from our laboratory -have shown that, in the TNBS and DSS models of colitis, there is a significant increase in the inflammatory Th17 subset in the colon and colonic-associated mesenteric lymph node (MLN) (21)(22)(23)(24), which plays a role in pathogenesis. To that end, we studied Th17/Treg subsets in the MLN and found that, in the TNBS + Vehicle group, there was a significant increase in the number of Th17 cells ( Figure 1G).…”

Section: Resultsmentioning

confidence: 88%

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Busbee¹,

Menzel²,

Alrafas³

et al. 2020

JCI Insight

101

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Section: Resultsmentioning

confidence: 88%

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Busbee¹,

Menzel²,

Alrafas³

et al. 2020

JCI Insight

101

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“…Even though B. vulgatus-colonization resulted in a slightly and nonsignificant increased induction of Bregs, the differentiation of T helper cells is not altered in comparison to germfree mice. In contrast, the significant enhanced induction of Bregs in vitro and in vivo in E. coli-associated mice leading to an anti-inflammatory balance of Th1/Th2/Th17/Treg cells, marked by a pronounced differentiation of Tregs, which is decisive for the development of inflammation and consequently the possible reason for the extenuated inflammation in E. coli-colonized and DSS treated mice (121)(122)(123).…”

Section: Discussionmentioning

confidence: 95%

“…In contrast, T cells incubated with E. coli-primed B cells favored a polarization shifted toward Th2 cells and Tregs. B. vulgatus-primed B cells also polarized T cells in a Th2 and Treg direction but simultaneously induced Th1 and Th17 cells leading to a more pro-inflammatory Th1/Th2/Th17/Treg balance (121)(122)(123). The cause for the strong T cell activation, proliferation and polarization by naïve unstimulated B cells could be the basic expression levels of MHC-II and co-stimulatory proteins in the absence of anti-inflammatory cytokines and surface molecules, which were upregulated in E. coli-primed B cells, as shown in previous experiments (124).…”

Section: Discussionmentioning

confidence: 98%

Bacterial Immunogenicity Is Critical for the Induction of Regulatory B Cells in Suppressing Inflammatory Immune Responses

et al. 2020

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B cells fulfill multifaceted functions that influence immune responses during health and disease. In autoimmune diseases, such as inflammatory bowel disease, multiple sclerosis and rheumatoid arthritis, depletion of functional B cells results in an aggravation of disease in humans and respective mouse models. This could be due to a lack of a pivotal B cell subpopulation: regulatory B cells (Bregs). Although Bregs represent only a small proportion of all immune cells, they exhibit critical properties in regulating immune responses, thus contributing to the maintenance of immune homeostasis in healthy individuals. In this study, we report that the induction of Bregs is differentially triggered by the immunogenicity of the host microbiota. In comparative experiments with low immunogenic Bacteroides vulgatus and strong immunogenic Escherichia coli, we found that the induction and longevity of Bregs depend on strong Toll-like receptor activation mediated by antigens of strong immunogenic commensals. The potent B cell stimulation via E. coli led to a pronounced expression of suppressive molecules on the B cell surface and an increased production of anti-inflammatory cytokines like interleukin-10. These bacteria-primed Bregs were capable of efficiently inhibiting the maturation and function of dendritic cells (DCs), preventing the proliferation and polarization of T helper (Th)1 and Th17 cells while simultaneously promoting Th2 cell differentiation in vitro. In addition, Bregs facilitated the development of regulatory T cells (Tregs) resulting in a possible feedback cooperation to establish immune homeostasis. Moreover, the colonization of germfree wild type mice with E. coli but not B. vulgatus significantly reduced intestinal inflammatory processes in dextran sulfate sodium (DSS)-induced colitis associated with an increase induction of immune suppressive Bregs. The quantity of Bregs directly correlated with the severity of inflammation. These findings may provide new insights and therapeutic approaches for B cell-controlled treatments of microbiota-driven autoimmune disease.

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“…However, it is now becoming more evident that the principal function of CCR6 in the gut mucosal compartment happens to be inducing leukocyte migration during inflammation, which in the absence of CCR6 is seemingly reduced and thus it is far better not to produce or promote excessive immune cell mobilization during colitis inflammation. Modulation of the CCR6-CCL20 function would be a worthwhile strategy that needs to be explored to produce a cure phenotype during both acute and chronic disease phases of colitis [29].…”

Section: Effect Of Chemokines (Ccr6 and Ccl20) On T Cells In Ibdmentioning

confidence: 99%

CCR6–CCL20 Axis in IBD: What Have We Learnt in the Last 20 Years?

Ranasinghe

Eri

2018

Gastrointestinal Disorders

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CC chemokine receptor 6 (CCR6) and its specific partner CC chemokine ligand 20 (CCL20) are known to play a pivotal role in intestinal inflammation. CCR6-associated inflammatory bowel disease (IBD) is already at the forefront of experimental inflammatory disease models, being the subject of numerous analytical studies. IBD is associated with two sub phenotypes, Crohn’s disease (CD) and ulcerative colitis (UC). Both these disease entities produce potent immune dysregulation followed by intense tissue damage within the gut mucosal system, initiating symptoms that are severely debilitating. Multiple causative factors are said to be responsible for IBD, but direct immune dysfunction is kindled by overplay of innate and adaptive immune responses produced against the luminal contents through the weakened or leaky gut epithelial barrier. Once immune homeostasis is not achieved by endogenous protective mechanisms, the self-assertive adaptive immunity mobilizes its various T and B cell cohorts, initializing their immune mechanisms by deploying the immune cells towards the site of infection. CCR6 and its unique solitary ligand CCL20 are small protein molecules that are abundantly expressed by T and B lymphocytes and act as chemotactic immune-modulatory envoys that help in the deployment of the effector lymphocyte arm of the immune system and produce two directly opposing outcomes in IBD. This dichotomous immunity consists of either immune tolerance or inflammation which then develops into a chronic state, remaining unresponsive to inherent immunity or targeted clinical therapy. In this review, we have identified large numbers of experimental studies that have employed both mouse models and clinical subjects spanning a period of nearly two decades and we have clustered these into 13 different groups. This review will provide greater understanding of the CCR6–CCL20 axis in IBD and identify gaps in the literature that can be filled in the future.

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Th1/Th2 Balance and Th17/Treg-Mediated Immunity in relation to Murine Resistance to Dextran Sulfate-Induced Colitis

Cited by 49 publications

References 43 publications

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner

Bacterial Immunogenicity Is Critical for the Induction of Regulatory B Cells in Suppressing Inflammatory Immune Responses

CCR6–CCL20 Axis in IBD: What Have We Learnt in the Last 20 Years?

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