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Related Concept Videos

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 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 Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...
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...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

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Isolation and Th17 Differentiation of Na&iuml;ve CD4 T Lymphocytes
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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

A protective function for interleukin 17A in T cell-mediated intestinal inflammation.

William O'Connor1, Masahito Kamanaka, Carmen J Booth

  • 1Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.

Nature Immunology
|May 19, 2009
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Interleukin-17A (IL-17A) plays a protective role in inflammatory bowel disease models. T cells producing IL-17A prevent severe colitis, highlighting IL-17A

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Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • Interleukin 23 (IL-23) and Interleukin-17 (IL-17) are implicated in chronic inflammatory diseases like inflammatory bowel disease (IBD).
  • The specific role of IL-17 in IBD pathogenesis remains incompletely understood, despite emerging functions for IL-23.

Purpose of the Study:

  • To elucidate the function of IL-17 in the context of inflammatory bowel disease.
  • To investigate the protective or detrimental effects of IL-17A signaling in a colitis model.

Main Methods:

  • Utilized the CD45RBhi T cell transfer model of colitis in mice.
  • Compared disease progression in mice receiving T cells deficient in IL-17A or IL-17 receptor.
  • Analyzed gene expression of T helper type 1 cytokines in colon tissue.
  • Assessed IL-17A's modulation of T helper type 1 polarization in vitro.

Main Results:

  • T cells lacking IL-17A led to an accelerated wasting disease, indicating a protective role for IL-17A.
  • Accelerated colitis correlated with increased expression of T helper type 1 cytokine genes in colon tissue.
  • IL-17A demonstrated an ability to modulate T helper type 1 polarization in vitro.
  • Mice receiving T cells deficient in the IL-17 receptor exhibited a more aggressive wasting disease.

Conclusions:

  • IL-17A exerts a protective function in the CD45RBhi transfer model of colitis.
  • T cells are identified as both a source and a target of IL-17 in vivo during inflammatory responses.