In this issue of Blood, Lim et al show that regulatory T cells (Tregs) from aplastic anemia (AA) patients are susceptible to Fas ligand (FasL)-mediated apoptosis, which may explain, in part, their diminution at disease onset.(1) The cell death can be overcome in vitro and in vivo by interleukin-2 (IL-2) supplemen-tation. This work builds on the previous observation of the same group, which showed 2 subpopulations of Tregs with distinct phenotypes in AA: Treg A, with a naive phenotype (low proliferative index), and Treg B, with a memory phenotype (moderate/high proliferative index) that correlated with response to immuno-suppressive therapy (IST).(2)
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