Fig. 2: The abnormal hematopoiesis-supporting ability and immunomodulatory function of BM EPCs from patients with AA can be improved by inhibiting TGF-β pathway via in vitro coculture systems.
From: TGF-β inhibition restores hematopoiesis and immune balance via bone marrow EPCs in aplastic anemia

a,b, The HSC EdU-positive ratio (a) and the CFU plating efficiency (b) of BM CD34+ cells from NCs after 5 days of coculture with cultivated AA EPCs or NC EPCs. c, Representative gating strategies of TH1 (CD3+CD8-IFN-γ+), TH2(CD3+CD8-IL-4+), and TH17 (CD3+CD8-IL-17+) cells among CD4+ T cells, as well as TC cells 1(CD3+CD8+IFN-γ+), TC2 (CD3+CD8+IL-4+), and TC17 (CD3+CD8+IL-17+) cells among CD8+ T cells via flow cytometry, after 3 days of coculture with AA EPCs or NC EPCs with or without TGF-βRI kinase inhibitor. d–j, The frequencies of BM TH1 cells among CD4+ T cells (d), TC1 cells among CD8+ T cells (e), TH2 cells among CD4+ T cells (f), TC2 cells among CD8+ T cells (g), TH17 cells among CD4+ T cells (h), TC17 cells among CD8+ T cells (i) and Treg (CD3+CD8−CD25+Foxp3+) among CD4+ T cells (j).