Horwitz David A, Zheng Song Guo, Gray J Dixon
Division of Rheumatology and Immunology, Department of Medicine, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA.
Trends Immunol. 2008 Sep;29(9):429-35. doi: 10.1016/j.it.2008.06.005. Epub 2008 Aug 3.
Foxp3(+) CD4(+) CD25(+) regulatory cell (Treg) subsets that maintain immunologic homeostasis have been considered to be a homogeneous population of naturally occurring, thymus-derived CD4(+)CD25(+) cells (nTregs). However, similar Foxp3+ Tregs can be induced from CD25(-) precursors in vivo, and ex vivo with interleukin 2 (IL-2) and transforming growth factor beta (TGF-beta) (iTregs). These two subsets differ in their principal antigen specificities and in the T-cell receptor signal strength and co-stimulatory requirements needed for their generation. However, whether iTregs have any unique functions in vivo has been unclear. Although IL-6 can convert nTregs to Th17 cells, iTregs induced by IL-2 and TGF-beta are resistant to this cytokine and thereby might retain suppressive function at inflammatory sites. Thus, nTregs and iTregs may have different roles in the adaptive immune response.
维持免疫稳态的Foxp3(+) CD4(+) CD25(+)调节性细胞(Treg)亚群曾被认为是天然存在的、源自胸腺的CD4(+)CD25(+)细胞(nTreg)的同质群体。然而,体内可从CD25(-)前体细胞诱导出类似的Foxp3+ Treg,体外利用白细胞介素2(IL-2)和转化生长因子β(TGF-β)也可诱导产生(iTreg)。这两个亚群在主要抗原特异性以及生成所需的T细胞受体信号强度和共刺激需求方面存在差异。然而,iTreg在体内是否具有任何独特功能尚不清楚。虽然IL-6可将nTreg转化为Th17细胞,但由IL-2和TGF-β诱导的iTreg对这种细胞因子具有抗性,因此可能在炎症部位保留抑制功能。因此,nTreg和iTreg在适应性免疫反应中可能具有不同作用。