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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...
Inflammatory Bowel Disease IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

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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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

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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...

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Related Experiment Video

Updated: Jul 19, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

Synergistic costimulation by both B7 molecules regulates colitis pathogenesis.

Gisen Kim1, Stephen P Schoenberger, Arlene Sharpe

  • 1La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA. mitch@liai.org

Annals of the New York Academy of Sciences
|October 24, 2006
PubMed
Summary

Surprisingly, blocking either B7-1 or B7-2 costimulation molecules accelerated colitis in mice. This suggests partial costimulation blockade can worsen autoimmune disease, contrary to expectations.

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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Area of Science:

  • Immunology
  • Autoimmunity
  • T cell costimulation

Background:

  • The roles of B7-1 (CD80) and B7-2 (CD86) in autoimmune pathogenesis are debated.
  • These molecules are critical for T cell activation and costimulation.
  • Understanding their specific contributions is vital for developing immunotherapies.

Purpose of the Study:

  • To investigate the in vivo roles of B7-1 and B7-2 in a mouse model of colitis.
  • To determine how the absence of either B7-1 or B7-2 affects T cell-mediated autoimmune disease.
  • To elucidate the impact of partial costimulation blockade on immune responses and disease severity.

Main Methods:

  • Induction of colitis via adoptive transfer of CD45RB(high) CD4+ T cells into immune-deficient (Rag(-/-)) recipients.
  • Analysis of Rag(-/-) recipients lacking either B7-1 or B7-2 expression.
  • In vitro assessment of T cell proliferation and cytokine production (IL-2) by antigen-presenting cells (APCs) deficient in B7 molecules.
  • Evaluation of regulatory T cell function and induction of CTLA-4.

Main Results:

  • Colitis onset and severity were significantly accelerated in Rag(-/-) recipients lacking either B7-1 or B7-2.
  • APCs deficient in B7-1 or B7-2 supported T cell proliferation but resulted in suboptimal IL-2 production and reduced CTLA-4 induction.
  • Regulatory T cell function appeared normal, but they could not counteract the heightened pathogenesis driven by T cells primed in B7-deficient environments.
  • The inhibitory function of CTLA-4 on pathogenic T cells was crucial in slowing colitis, even without effective regulatory T cells.

Conclusions:

  • Partial blockade of B7 costimulation, by lacking either B7-1 or B7-2, unexpectedly augments autoimmune colitis.
  • The findings highlight a complex role for B7 molecules, where their absence can exacerbate disease.
  • Complete costimulation blockade might prevent autoimmunity, but partial blockade may worsen it in certain contexts.