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Related Concept Videos

Antigens Involved in Adaptive Immunity01:26

Antigens Involved in Adaptive Immunity

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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
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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...
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MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
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The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
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Updated: Aug 15, 2025

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Intestinal epithelial HDAC3 and MHC class II coordinate microbiota-specific immunity.

Emily M Eshleman1,2, Tzu-Yu Shao2,3,4, Vivienne Woo1,2

  • 1Division of Immunobiology.

The Journal of Clinical Investigation
|January 5, 2023
PubMed
Summary

Epithelial histone deacetylase 3 (HDAC3) controls gut immunity by regulating T cells. Loss of HDAC3 in epithelial cells promotes T cell accumulation and inflammation, highlighting its role in maintaining immune balance against gut microbes.

Keywords:
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Area of Science:

  • Immunology
  • Microbiology
  • Gastroenterology

Background:

  • Aberrant immune responses to gut microbes drive inflammatory bowel disease.
  • Control mechanisms for microbiota-specific immunity in mucosal tissues are not well understood.

Purpose of the Study:

  • To investigate the role of epithelial histone deacetylase 3 (HDAC3) in instructing microbiota-specific immunity.
  • To understand how epithelial HDAC3 influences CD4+ T cell populations and intestinal inflammation.

Main Methods:

  • Mice lacking epithelial HDAC3 were used to study microbiota-specific immunity.
  • Analysis of CD4+ T cell subsets (Tregs, Th17) and epithelial MHC class II (MHCII) expression.
  • Investigated the NF-κB signaling pathway's role in HDAC3-mediated MHCII regulation.

Main Results:

  • Epithelial HDAC3 deficiency led to increased commensal-specific CD4+ T cells in the intestine.
  • Loss of epithelial HDAC3 decreased regulatory T cells (Tregs) and increased Th17 cells, promoting colitis.
  • HDAC3 is crucial for NF-κB-dependent epithelial MHCII expression, which limits Th17 cells and protects against inflammation.

Conclusions:

  • Epithelial HDAC3 plays a critical role in balancing microbiota-specific CD4+ T cell subsets in the intestine.
  • HDAC3-mediated regulation of epithelial MHCII is essential for controlling T cell responses to commensal microbes.
  • These findings reveal a novel mechanism by which epithelial cells shape mucosal immunity and prevent chronic inflammation.