期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 14, 页码 -出版社
MDPI
DOI: 10.3390/ijms22147522
关键词
influenza A virus; Tregs; lung; inflammation; methylation; Tbx21; Foxp3
资金
- German Academic Exchange Service (DAAD) [57129429]
- Helmholtz-Gemeinschaft, Zukunftsthema Immunology and Inflammation [ZT-0027]
The research revealed that T cell subsets accumulation in IAV-infected lungs is transient, while the change in the ratio of CD4(+) to CD8(+) T cells is more durable. Tregs co-expressing T-bet peak at Day 7 post-infection, showing a strong demethylated characteristic.
During influenza A virus (IAV) infections, CD4(+) T cell responses within infected lungs mainly involve T helper 1 (Th1) and regulatory T cells (Tregs). Th1-mediated responses favor the co-expression of T-box transcription factor 21 (T-bet) in Foxp3(+) Tregs, enabling the efficient Treg control of Th1 responses in infected tissues. So far, the exact accumulation kinetics of T cell subsets in the lungs and lung-draining lymph nodes (dLN) of IAV-infected mice is incompletely understood, and the epigenetic signature of Tregs accumulating in infected lungs has not been investigated. Here, we report that the total T cell and the two-step Treg accumulation in IAV-infected lungs is transient, whereas the change in the ratio of CD4(+) to CD8(+) T cells is more durable. Within lungs, the frequency of Tregs co-expressing T-bet is steadily, yet transiently, increasing with a peak at Day 7 post-infection. Interestingly, T-bet(+) Tregs accumulating in IAV-infected lungs displayed a strongly demethylated Tbx21 locus, similarly as in T-bet(+) conventional T cells, and a fully demethylated Treg-specific demethylated region (TSDR) within the Foxp3 locus. In summary, our data suggest that T-bet(+) but not T-bet(-) Tregs are epigenetically stabilized during IAV-induced infection in the lung.
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