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Updated: Jun 3, 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
Microbiota: dual-faceted player in experimental colitis
Ting Feng1, Charles O Elson, Yingzi Cong
1Department of Microbiology, University of Texas Medical Branch, Galveston, TX, USA.
Gut Microbes
|April 7, 2011
Summary
Microbiota drives chronic intestinal inflammation by stimulating innate immunity, leading to T cell proliferation. This process requires both microbial signals and antigen recognition for colitis development.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Microbiota stimulation of innate immune pathways is crucial for T cell proliferation and chronic intestinal inflammation.
- Dendritic cells activated by microbiota produce interleukin-6 (IL-6) via a Toll-like receptor/MyD88-dependent pathway, promoting T cell proliferation.
Purpose of the Study:
- To investigate the role of microbiota in T cell spontaneous proliferation and the development of chronic intestinal inflammation.
- To determine the specific mechanisms by which microbiota induces colitis.
Main Methods:
- Utilized T cell receptor transgenic (Tg) mice (CBir1 Tg and OT-II T cells) in adoptive transfer experiments.
- Administered specific pathogen-free RAG(-/-) mice with T cells.
- Employed blockade of IL-6 to assess its role in colitis induction.
Main Results:
- While both CBir1 Tg and OT-II T cells proliferated spontaneously, only CBir1 Tg T cells induced colitis in recipient mice.
- Blocking IL-6 or IL-6-mediated proliferation of CBir1 Tg T cells abrogated colitis induction.
- Microbiota acts as a natural adjuvant for T cell spontaneous proliferation and chronic intestinal inflammation.
Conclusions:
- Both microbiota stimulation of innate immune cells and microbiota antigen activation of T cells are essential for experimental colitis.
- Microbiota-induced IL-6 production by dendritic cells is a key pathway for T cell proliferation and colitis development.
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