par Englebert, Kevin ;Taquin, Anaëlle ;Azouz, Abdulkader ;Acolty, Valérie ;Vande Velde, Sylvie ;Vanhollebeke, Marie ;Innes, Hadrien;Boon, Louis;Keler, Tibor;Leo, Oberdan;Goriely, Stanislas ;Moser, Muriel ;Oldenhove, Guillaume
Référence Cell reports, 43, 3, page (113824)
Publication Publié, 2024-03-01
Référence Cell reports, 43, 3, page (113824)
Publication Publié, 2024-03-01
Article révisé par les pairs
Résumé : | Adipose tissue homeostasis relies on the interplay between several regulatory lineages, such as type 2 innate lymphoid cells (ILC2s), T helper 2 (Th2) cells, regulatory T cells, eosinophils, and type 2 macrophages. Among them, ILC2s are numerically the dominant source of type 2 cytokines and are considered as major regulators of adiposity. Despite the overlap in immune effector molecules and sensitivity to alarmins (thymic stromal lymphopoietin and interleukin-33) between ILC2s and resident memory Th2 lymphocytes, the role of the adaptive axis of type 2 immunity remains unclear. We show that mice deficient in CD27, a member of the tumor necrosis factor receptor superfamily, are more resistant to obesity and associated disorders. A comparative analysis of the CD4 compartment of both strains revealed higher numbers of fat-resident memory Th2 cells in the adipose tissue of CD27 knockout mice, which correlated with decreased programmed cell death protein 1-induced apoptosis. Our data point to a non-redundant role for Th2 lymphocytes in obesogenic conditions. |