We infected mice with the mouse cytomegalovirus (MCMV) that colonizes most of the tissues and organs including the small intestine. TCRαβ CD8αβ IELs exhibited the highest proliferation, T-bet expression, and a proportion of them are virus-specific CD8 T cells. These TCRαβ CD8αβ IELs mirror TCRαβ CD8αβ cells in the spleen during MCMV infection, raising questions about their origin.
We also examined surface receptors on IELs linked to MCMV infection and activation. KLRG1 was highly expressed across IEL subsets. 2B4 (CD244) and NKG2D were highly expressed on TCRαβ CD8αα IELs. Surprisingly, by surface staining I found that all IEL subsets expressed chemokine CCL5, unlike TCRαβ CD8αβ T cells in the spleen, indicating small intestine-specific regulation. The expression of this activation receptors and expression of chemokine CCL5 on the surface of all subset of IELs suggests that MCMV could have a role in the regulation of all three subtypes of IELs. Interestingly, lipid droplet formation was increased in spleen CD8 T cells but decreased in IELs during MCMV infection. These findings require further studies on lipid droplet production by other immune cell types, particularly with regard to the role of the unique environment of the small intestine on IELs.
Mitochondrial staining remained unaffected during MCMV infection, possibly due to distinct metabolic pathways triggered by this virus compared to other pathogens. High-fat diet experiments showed IEL activation without affecting virus-infected and non-infected mice, requiring further testing.
In conclusion, comparing impact of systemic infection on CD8 T cells in the spleen and small intestine during MCMV infection provided valuable insights for future research.
