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Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
T Cell Types and Functions01:24

T Cell Types and Functions

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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...
Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation. 
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...

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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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IL-27 promotes T cell-dependent colitis through multiple mechanisms.

Jennifer H Cox1, Noelyn M Kljavin, Nandhini Ramamoorthi

  • 1Department of Molecular Biology, Genentech Inc., South San Francisco, CA 94080, USA.

The Journal of Experimental Medicine
|December 22, 2010
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Interleukin-27 (IL-27) unexpectedly promotes intestinal inflammation by suppressing regulatory T cell development. Blocking IL-27 signaling may treat immune tolerance breakdown and colitis.

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Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells
06:57

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

Published on: September 18, 2016

Area of Science:

  • Immunology
  • Cytokine Signaling
  • Gastroenterology

Background:

  • Interleukin-27 (IL-27) is a cytokine with known dual roles in immunity.
  • Its immunoregulatory functions, like suppressing TH17 cells and promoting Tr1 cells, are often dominant in vivo.
  • IL-27 receptor alpha (Il27ra)-deficient mice exhibit heightened susceptibility to immune pathology.

Purpose of the Study:

  • To investigate the role of IL-27 in T cell-mediated colitis.
  • To clarify the controversial functions of IL-27 in experimental colitis models.
  • To determine if IL-27 signaling impacts regulatory T cell differentiation and function.

Main Methods:

  • Utilized a mouse T cell transfer model of colitis.
  • Generated Il27ra-deficient T cells for transfer.
  • Assessed weight loss, colonic inflammation, T cell phenotype (Foxp3 expression), and cytokine production (IFN-γ).
  • Conducted in vitro suppression assays for Foxp3 induction and an in vivo ovalbumin tolerization model.

Main Results:

  • Absence of Il27ra on transferred T cells led to reduced weight loss and colonic inflammation.
  • Il27ra-deficient T cells showed increased Foxp3 expression, indicating enhanced regulatory T cell differentiation.
  • IL-27 suppressed Foxp3 induction in vitro and in an ovalbumin-dependent tolerization model.
  • Effector T cell proliferation and IFN-γ production were diminished without Il27ra.

Conclusions:

  • IL-27 plays a proinflammatory role in T cell-dependent intestinal inflammation.
  • IL-27 restrains the development of regulatory T cells (Tregs).
  • Targeting IL-27 may be a therapeutic strategy for conditions involving a loss of peripheral immune tolerance.