| Autor: |
Quintana, Juan F., Sinton, Matthew C., Chandrasegaran, Praveena, Lestari, Agatha Nabilla, Heslop, Rhiannon, Cheaib, Bachar, Ogunsola, John, Ngoyi, Dieudonne Mumba, Kuispond Swar, Nono-Raymond, Cooper, Anneli, Mabbott, Neil A., Coffelt, Seth B., MacLeod, Annette |
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| Zdroj: |
Nature Communications; 8/29/2023, Vol. 14 Issue 1, p1-17, 17p |
| Abstrakt: |
African trypanosomes colonise the skin to ensure parasite transmission. However, how the skin responds to trypanosome infection remains unresolved. Here, we investigate the local immune response of the skin in a murine model of infection using spatial and single cell transcriptomics. We detect expansion of dermal IL-17A-producing Vγ6+ cells during infection, which occurs in the subcutaneous adipose tissue. In silico cell-cell communication analysis suggests that subcutaneous interstitial preadipocytes trigger T cell activation via Cd40 and Tnfsf18 signalling, amongst others. In vivo, we observe that female mice deficient for IL-17A-producing Vγ6+ cells show extensive inflammation and limit subcutaneous adipose tissue wasting, independently of parasite burden. Based on these observations, we propose that subcutaneous adipocytes and Vγ6+ cells act in concert to limit skin inflammation and adipose tissue wasting. These studies provide new insights into the role of γδ T cell and subcutaneous adipocytes as homeostatic regulators of skin immunity during chronic infection. Trypansome brucei infection can result in colonisation of the skin but how this impacts the skin architecture and immune response has not been fully resolved. Here the authors apply a spatially resolved single cell transcriptomics approach in a murine model of infection, and suggest a role for IL-17- producing γδ T cells in the immune response to T. brucei skin infection. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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