Regulatory T Cells and Immune Tolerance in the Intestine

Harrison, O. J.; Powrie, F. M.

doi:10.1101/cshperspect.a021022

Cited by 22 publications

(29 citation statements)

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“…Maintaining homeostasis in the gut is a crucial balancing act providing tolerance to important beneficial microbes and resisting potential pathogenic microbes, and one that rest on the ability of the immune system to make this distinction and respond appropriately. Traditionally, the transcription factor RORγt is expressed and involved in the differentiation of T H 17 cells while Foxp3 is involved in regulatory T cell differentiation (Korn et al 2009, Harrison and Powrie 2013). However, recent studies have also found populations of T cells in the gut that express both Rorγt and Foxp3, produce the regulatory cytokine IL-10 instead of IL-17 and are functionally equivalent to Tregs (Lochner et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Differential immune responses and microbiota profiles in children with autism spectrum disorders and co-morbid gastrointestinal symptoms

Rose

Yang

Serena

et al. 2018

Brain, Behavior, and Immunity

163

177

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Section: Discussionmentioning

confidence: 99%

Differential immune responses and microbiota profiles in children with autism spectrum disorders and co-morbid gastrointestinal symptoms

Rose

Yang

Serena

et al. 2018

Brain, Behavior, and Immunity

163

177

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“…iT reg cells are essential for maintaining immune homeostasis, especially at mucosal interfaces; additionally iT reg cells contribute to fetal tolerance 5,12,13. In the gut, naive CD4 + T cells are converted into iT reg cell following TCR stimulation in the presence of TGF-β and IL-2; other compounds such as retinoic acid (RA) or short-chain-fatty-acids from microbiota mediate conversion as well 7. IL-10 is also a key player in maintaining lymphocyte homeostasis in the gut as IL-10 deficient mice suffer from spontaneous colitis 7.…”

Section: Discussionmentioning

confidence: 99%

“…In the gut, naive CD4 + T cells are converted into iT reg cell following TCR stimulation in the presence of TGF-β and IL-2; other compounds such as retinoic acid (RA) or short-chain-fatty-acids from microbiota mediate conversion as well 7. IL-10 is also a key player in maintaining lymphocyte homeostasis in the gut as IL-10 deficient mice suffer from spontaneous colitis 7. Our results clearly show that Triple lo T reg cells suppress colitis induction.…”

Section: Discussionmentioning

confidence: 99%

Affinity for self antigen selects Treg cells with distinct functional properties

et al. 2016

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How regulatory T cells (Treg cell) control lymphocyte homeostasis is not fully understood. Here we identify two Treg cell populations with differing degrees of self-reactivity and distinct regulatory functions. Triplehi (GITRhiPD-1hiCD25hi) Treg cell are highly self-reactive and control lympho-proliferation in peripheral lymph nodes. Triplelo (GITRloPD-1loCD25lo) Treg cells are less self-reactive and limit development of colitis by promoting conversion of CD4+ Tconv cells into induced Treg cells (iTreg cells). Although Foxp3-deficient (scurfy) mice lack Treg cells, they contain Triplehi-like and Triplelo-like CD4+ T cells with distinct pathological properties. Scurfy TriplehiCD4+T cells infiltrate the skin whereas scurfy TripleloCD4+T cells induce colitis and wasting disease. These findings indicate that T cell receptor affinity for self-antigens drives the differentiation of Tregs into distinct subsets with non-overlapping regulatory activities.

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“…A correlation was noted between the toxicity of CPT-11 and the elevation of pro-inflammation cytokines, but the impact of immune tolerance was not investigated in this study. It is known that the CD4 + Foxp3 + regulatory T cells (Treg cells) and IL-10 producing CD4 + T cells play a critical role in maintaining immune tolerance in the mucosa (Annacker et al , 2003; Konkel et al , 2011; Harrison et al , 2013). TCRαβ + CD8αα + unconventional T cells in intraepithelial lymphocytes can also maintain the immune balance in intestine (Poussier et al , 2002).…”

Section: Discussionmentioning

confidence: 99%

Irinotecan (CPT-11)-induced elevation of bile acids potentiates suppression of IL-10 expression

Fang

Zhang

Cao

et al. 2016

Toxicology and Applied Pharmacology

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Irinotecan (CPT-11) is a first-line anti-colon cancer drug, however; CPT-11-induced toxicity remains a key factor limiting its clinical application. To search for clues to the mechanism of CPT-11-induced toxicity, metabolomics was applied using ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight mass spectrometry. Intraperitoneal injection of 50 mg/kg of CPT-11 induced loss of body weight, and intestine toxicity. Changes in gallbladder morphology suggested alterations in bile acid metabolism, as revealed at the molecular level by analysis of the liver, bile, and ileum metabolomes between the vehicle-treated control group and the CPT-11-treated group. Analysis of immune cell populations further showed that CPT-11 treatment significantly decreased the IL-10-producing CD4 T cell frequency in intestinal lamina propria lymphocytes, but not in spleen or mesenteric lymph nodes. In vitro cell culture studies showed that the addition of bile acids deoxycholic acid and taurodeoxycholic acid accelerated the CPT-11-induced suppression of IL-10 secretion by activated CD4+ naive T cells isolated from mouse splenocytes. These results showed that CPT-11 treatment caused metabolic changes in the composition of bile acids that altered CPT-11-induced suppression of IL-10 expression.

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Regulatory T Cells and Immune Tolerance in the Intestine

Cited by 22 publications

References 0 publications

Differential immune responses and microbiota profiles in children with autism spectrum disorders and co-morbid gastrointestinal symptoms

Differential immune responses and microbiota profiles in children with autism spectrum disorders and co-morbid gastrointestinal symptoms

Affinity for self antigen selects Treg cells with distinct functional properties

Irinotecan (CPT-11)-induced elevation of bile acids potentiates suppression of IL-10 expression

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