Moqian Zheng

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).

Abstract Steroid-refractory gut acute graft-versus-host disease (SR-Gut-aGVHD) is the major cause of nonrelapse death after allogeneic hematopoietic cell transplantation. High numbers of donor-type IL-22+ T cells, IL-22–dependent dysbiosis, and loss of antiinflammatory CX3CR1hi mononuclear phagocytes (MNPs) play critical roles in SR-Gut-aGVHD pathogenesis. CEACAM1 on intestinal epithelial cells (IECs) is proposed to regulate bacterial translocation and subsequent immune responses in the intestine.