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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Inflammatory Bowel Disease II: Crohn's Disease01:30

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Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
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Chronic Bowel Disorders: Introduction01:17

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Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
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Updated: Sep 28, 2025

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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RORγt-Expressing Pathogenic CD4+ T Cells Cause Brain Inflammation during Chronic Colitis.

Michel Edwar Mickael1, Suniti Bhaumik1, Ayanabha Chakraborti2

  • 1Department of Pathology, University of Alabama at Birmingham, Birmingham, AL.

Journal of Immunology (Baltimore, Md. : 1950)
|April 5, 2022
PubMed
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Pathogenic CD4+ T cells expressing RORγt drive brain inflammation and neurobehavioral disorders in inflammatory bowel disease. Reducing these cells ameliorates brain pathology, linking gut inflammation to neurological dysfunction.

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Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells
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Area of Science:

  • Immunology
  • Neuroscience
  • Gastroenterology

Background:

  • Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is associated with neurobehavioral disorders and brain abnormalities.
  • The precise mechanisms underlying these neurological complications in IBD remain unclear.
  • CD4+ T cell subsets, particularly Th17 cells, are implicated in neuroinflammatory and cognitive conditions like multiple sclerosis and Alzheimer's disease.

Purpose of the Study:

  • To investigate the role of CD4+ T lymphocytes in the development of brain pathology during chronic intestinal inflammation.
  • To elucidate the contribution of Th17 cells to neuroinflammation and associated neurobehavioral disorders in a mouse model of colitis.

Main Methods:

  • Utilized a T cell transfer model of chronic colitis in Rag1-/- mice.
  • Analyzed CD4+ T cell infiltration into the brain and correlated it with colitis severity and neurobehavioral deficits.
  • Investigated the phenotype of brain-infiltrating CD4+ T cells, focusing on the Th17 transcription factor RORγt.
  • Performed adoptive transfer experiments using RORγt-deficient CD4+ T cells.
  • Examined dextran sulfate sodium-induced colitis in Rorc mutant mice.

Main Results:

  • CD4+ T cells infiltrated the brain of colitic mice in proportion to colitis severity.
  • Colitic mice exhibited hypothalamic astrogliosis and neurobehavioral disorders.
  • Brain-infiltrating CD4+ T cells expressed RORγt and exhibited a pathogenic Th17 phenotype.
  • Transfer of RORγt-deficient CD4+ T cells prevented brain inflammation and neurobehavioral deficits.
  • Rorc mutant mice showed reduced brain inflammation and astrogliosis despite more severe colitis.

Conclusions:

  • Pathogenic RORγt+ CD4+ T cells, implicated in colitis exacerbation, preferentially migrate to the brain.
  • These cells contribute to brain inflammation and neurobehavioral disorders in the context of IBD.
  • The findings establish a direct link between gut inflammation severity and neuroinflammation mediated by specific T cell populations.