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Published on: December 16, 2021
IL-33 Increases the Magnitude of the Tissue-Resident Memory T Cell Response in Intestinal Tissues during Local
Giuseppina Marchesini Tovar1, Angie M Espinal1, Corey Gallen1
1Department of Pathology, Immunology and Laboratory Medicine, Center for Immunity and Inflammation, Rutgers New Jersey Medical School, Rutgers-The State University of New Jersey, Newark, NJ.
Interleukin-33 (IL-33) signaling enhances T cell numbers and commitment to intestinal tissue residency during Yersinia pseudotuberculosis infection in mice. Blocking IL-33 did not affect memory T cell generation but ST2 overexpression increased T cell numbers.
Area of Science:
- Immunology
- Microbiology
- T cell biology
Background:
- Interleukin-33 (IL-33) is crucial for early CD8 T cell programming.
- The role of IL-33 in generating tissue-resident memory T cells in vivo is not well understood.
Purpose of the Study:
- To investigate the role of IL-33 signaling in the differentiation and maintenance of tissue-resident memory T cells in the intestine.
- To determine the impact of IL-33/ST2 axis on T cell responses during Yersinia pseudotuberculosis infection.
Main Methods:
- Infection of mice with Yersinia pseudotuberculosis.
- Analysis of IL-33 and ST2 expression in intestinal tissues and T cells.
- Blocking IL-33 signaling and overexpression of ST2 on T cells.
Main Results:
- IL-33 expression increased in the intestine post-infection, coinciding with ST2 expression on infiltrating T cells.
- Blocking IL-33 signaling did not significantly alter the number or phenotype of generated tissue-resident memory T cells.
- ST2 overexpression on T cells increased TCF1 expression and T cell numbers in the intestine, though these effects were transient.
Conclusions:
- IL-33 signaling promotes T cell accumulation and commitment to intestinal tissue residency during infection.
- While not essential for initial memory T cell generation, IL-33 influences T cell numbers and residency in the gut.
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