Sinton M. C. auteur aut IRD Chandrasegaran P. R. G. auteur aut IRD Capewell P. auteur aut IRD Cooper A. auteur aut IRD Girard A. auteur aut IRD Ogunsola J. auteur aut IRD Perona-Wright G. auteur aut IRD Ngoyi D. auteur aut IRD Kuispond N. auteur aut IRD Bucheton Bruno auteur aut IRD Camara M. auteur aut IRD Kajimura S. auteur aut IRD Bénézech C. auteur aut IRD Mabbott N. A. auteur aut IRD MacLeod A. auteur aut IRD Quintana J. F. auteur aut IRD text journalArticle eng text/pdf reformatted digital access In the skin, Trypanosoma brucei colonises the subcutaneous white adipose tissue, and is proposed to be competent for forward transmission. The interaction between parasites, adipose tissue, and the local immune system is likely to drive the adipose tissue wasting and weight loss observed in cattle and humans infected with T. brucei. However, mechanistically, events leading to subcutaneous white adipose tissue wasting are not fully understood. Here, using several complementary approaches, including mass cytometry by time of flight, bulk and single cell transcriptomics, and in vivo genetic models, we show that T. brucei infection drives local expansion of several IL-17A-producing cells in the murine WAT, including TH17 and V gamma 6+ cells. We also show that global IL-17 deficiency, or deletion of the adipocyte IL-17 receptor protect from infection-induced WAT wasting and weight loss. Unexpectedly, we find that abrogation of adipocyte IL-17 signalling results in a significant accumulation of Dpp4+Pi16+ interstitial preadipocytes and increased extravascular parasites in the WAT, highlighting a critical role for IL-17 signalling in controlling preadipocyte fate, subcutaneous WAT dynamics, and local parasite burden. Taken together, our study highlights the central role of adipocyte IL-17 signalling in controlling WAT responses to infection, suggesting that adipocytes are critical coordinators of tissue dynamics and immune responses to T. brucei infection. specialized 052 020 080 14 1 7070 [21 ] [+ Correction, 1 p.] 2023 https://www.documentation.ird.fr/hor/fdi:010089652 10.1038/s41467-023-42918-8 [F B010089652] https://www.documentation.ird.fr/hor/fdi:010089652 https://horizon.documentation.ird.fr/exl-doc/pleins_textes/2024-04/010089652.pdf IRD - Base Horizon / Pleins textes 2024-04-05 2026-07-21 fdi:010089652 fre