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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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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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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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The Transcription Factor RXRα in CD11c+ APCs Regulates Intestinal Immune Homeostasis and Inflammation.

Indumathi Manoharan1,2, Arulkumaran Shanmugam1, Malarvizhi Ramalingam1

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Journal of Immunology (Baltimore, Md. : 1950)
|July 21, 2023
PubMed
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Retinoid X receptor alpha (RXRα) in antigen-presenting cells (APCs) is crucial for maintaining intestinal immune balance. Activating RXRα signaling suppresses inflammation, offering a potential therapeutic target for colitis.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • Antigen-presenting cells (APCs) are key in immune tolerance and intestinal homeostasis.
  • Molecular regulators that program APCs towards a regulatory or inflammatory state are largely unknown.

Purpose of the Study:

  • To investigate the role of retinoid X receptor alpha (RXRα) signaling in CD11c+ APCs for intestinal immune regulation.
  • To determine if RXRα programming of APCs influences inflammatory responses in the gut.

Main Methods:

  • Utilized a mouse model of ulcerative colitis.
  • Performed targeted deletion of RXRα in CD11c+ APCs.
  • Administered pharmacological activation of the RXRα pathway.

Main Results:

  • RXRα deletion in CD11c+ APCs exacerbated colitis, disrupting T cell homeostasis and increasing inflammation.
  • Loss of RXRα led to increased pro-inflammatory cytokines (Th1/Th17) and decreased regulatory T cell differentiation.
  • Pharmacological RXRα activation reduced colitis severity by suppressing inflammatory cytokines and Th1/Th17 responses.

Conclusions:

  • RXRα signaling in intestinal APCs is essential for maintaining immune homeostasis and suppressing inflammation.
  • Targeting the RXRα pathway presents a potential therapeutic strategy for inflammatory bowel diseases like colitis.