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Updated: Jun 1, 2026
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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
Published on: December 16, 2021
Intestinal bacterial colonization induces mutualistic regulatory T cell responses
Markus B Geuking1, Julia Cahenzli, Melissa A E Lawson
1Maurice Müller Laboratories (DKF), Universitätsklinik für Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, Bern, Switzerland. geuking@dkf.unibe.ch
Immunity
|May 21, 2011
Summary
Gut microbes promote the development of regulatory T (Treg) cells, crucial for preventing intestinal inflammation. This host-microbial adaptation ensures immune balance and gut homeostasis.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Mammals host a rich colonic microbiota influencing the immune system.
- Regulatory T (Treg) cells modulate microbe-induced intestinal inflammation.
- Distinguishing true mutualistic immune adaptation from idiosyncratic responses is challenging.
Purpose of the Study:
- To investigate mutualistic CD4+ T cell adaptation to the gut microbiota.
- To understand the role of Treg cells in host-microbial symbiosis.
Main Methods:
- Utilized the altered Schaedler flora (ASF) model in mammals.
- Assessed Treg cell activation and generation upon intestinal colonization.
- Evaluated T helper 17 (Th17) and T helper 1 (Th1) cell responses.
Main Results:
- Intestinal colonization with ASF induced colonic Treg cell activation and generation.
- Lack of Treg cell activation led to Th17 and Th1 cell responses.
- Wild-type Treg cells reversed these inflammatory responses.
- Treg cell induction was essential for maintaining intestinal homeostasis after dextran sulfate sodium-induced damage.
Conclusions:
- Microbiota colonization induces Treg cell responses as a fundamental mechanism for host-intestinal microbial mutualism.
- Treg cells are critical for maintaining intestinal homeostasis and preventing inflammation.
- This study elucidates a key adaptive immune mechanism governing the gut microbiome.
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