Joey Li

Abstract Pathogenic CD4+ memory T cells (Tm) sustain chronic inflammation, but mechanisms remain undefined. Here, we identify four donor-type CD4+ Tm subsets in the target tissues of autoimmune-like chronic graft-versus-host disease in mice: Ly108+CD69− stem-like memory T cells (Tsm), Ly108+CD69+ resident memory progenitor T cells (Trmp), Ly108−CD69+ terminally differentiated tissue-resident T cells (Trm), and Ly108−CD69− intermediate T cells (Tint).

Keywords natural killer cells unfolded protein response proteostasis dysfunction solid tumors Fli1 metabolism protein aggregate tumor interstitial fluid tumor microenvironment Get full text access Log in, subscribe or purchase for full access. References 1. Lanier, L.L. Evolutionary struggles between NK cells and viruses Nat. Rev. Immunol. 2008; 8:259-268 2. Li, J.H. ∙ O’Sullivan, T.E. Back to the Future: Spatiotemporal Determinants of NK Cell Antitumor Function Front. Immunol. 2022; 12, 816658 3.

Abstract Immune cells undergo rapid metabolic reprogramming to fuel effector responses. However, whether the metabolic pathways that supply these functions differ between human and mouse immune cells is poorly understood. Using a comparative metabolomics approach, here we show both conserved and species-distinct metabolite alterations in cytokine-activated primary human and mouse natural killer (NK) cells.