| First Author | Quintana JF | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 5279 |
| PubMed ID | 37644007 | Mgi Jnum | J:357223 |
| Mgi Id | MGI:7527933 | Doi | 10.1038/s41467-023-40962-y |
| Citation | Quintana JF, et al. (2023) gammadelta T cells control murine skin inflammation and subcutaneous adipose wasting during chronic Trypanosoma brucei infection. Nat Commun 14(1):5279 |
| abstractText | 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 Vgamma6(+) 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 Vgamma6(+) cells show extensive inflammation and limit subcutaneous adipose tissue wasting, independently of parasite burden. Based on these observations, we propose that subcutaneous adipocytes and Vgamma6(+) cells act in concert to limit skin inflammation and adipose tissue wasting. These studies provide new insights into the role of gammadelta T cell and subcutaneous adipocytes as homeostatic regulators of skin immunity during chronic infection. |
