Sloan-Lancaster J, Evavold B D, Allen P M
Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110.
J Exp Med. 1994 Oct 1;180(4):1195-205. doi: 10.1084/jem.180.4.1195.
We have demonstrated Th2 clonal anergy as a consequence of partial T cell activation by immunogenic peptide and chemically fixed APC, as well as by altered peptide ligand and live antigen-presenting cells (APC). Either stimulation resulted in a profound inability of the T cells to proliferate upon restimulation with antigen and functional APC, a similar phenomenon to that found with Th1 cells. The anergic state was long lasting and was restricted to proliferation, since the T cells retained the ability to produce cytokines upon restimulation, albeit at slightly reduced levels. Th2 anergy induction was inhibited by cyclosporine A, but not by provision of exogenous costimulation or growth factors. The data presented unify Th1 and Th2 cells with regard to anergy and suggest that the fundamental control during anergy for both subsets is prevention of clonal expansion, thus blocking amplification of the immune response.
我们已经证明,免疫原性肽和化学固定的抗原呈递细胞(APC),以及改变的肽配体和活的抗原呈递细胞(APC)引起的部分T细胞活化会导致Th2克隆无能。这两种刺激都会导致T细胞在用抗原和功能性APC再次刺激时严重无法增殖,这一现象与Th1细胞类似。无反应状态持续时间长且仅限于增殖,因为T细胞在再次刺激时仍保留产生细胞因子的能力,尽管水平略有降低。环孢素A可抑制Th2无反应性的诱导,但提供外源性共刺激或生长因子则不能。所呈现的数据在无反应性方面统一了Th1和Th2细胞,并表明两个亚群在无反应性期间的基本控制是防止克隆扩增,从而阻断免疫反应的放大。