Gαi2−/− Mice and Their Regulatory T Cells in Colitis
Author Information
Author(s): Götlind Yu-Yuan C., Raghavan Sukanya, Bland Paul W., Hörnquist Elisabeth Hultgren
Primary Institution: University of Gothenburg
Hypothesis
Is colitis in Gαi2−/− mice a consequence of a defect in CD4+FoxP3+ regulatory T cells?
Conclusion
Gαi2−/− Treg are functionally active but cannot prevent colitis due to the heightened activity of Gαi2−/− effector T cells.
Supporting Evidence
- Gαi2−/− mice develop colitis characterized by a Th1 CD4+ T cell response.
- Treg from Gαi2−/− mice are present at higher frequencies in inflamed tissues.
- Despite increased Treg numbers, Gαi2−/− effector T cells are less susceptible to suppression.
Takeaway
The study found that even though certain immune cells in mice with a specific genetic change are present in higher numbers, they can't stop the disease from happening.
Methodology
Flow cytometry and in vitro co-culture systems were used to analyze Treg and Teff cell functions.
Limitations
The study primarily focuses on a specific mouse model, which may not fully represent human conditions.
Participant Demographics
Mice used were Gαi2−/− and wild-type controls, aged 5-9 weeks.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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