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Natural and TGF-β–induced Foxp3+CD4+ CD25+ regulatory T cells are not mirror images of each other

2008; Elsevier BV; Volume: 29; Issue: 9 Linguagem: Inglês

10.1016/j.it.2008.06.005

1471-4981

David A. Horwitz, Song Guo Zheng, J. Dixon Gray,

Immunotherapy and Immune Responses

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 β (TGF-β) (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-β 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. 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 β (TGF-β) (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-β 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.