IngentaConnect Cooperation of invariant NKT cells and CD4CD25 T regulatory cells...

Authors: Li, Weipeng; Ji, Fang; Zhang, Yong¹; Wang, Ying¹; Yang, Neng¹; Ge, Hailiang¹; Wang, Fuqing

Source: Acta Biochimica et Biophysica Sinica, Volume 40, Number 5, May 2008 , pp. 381-390(10)

Abstract:

CD1d-restricted natural killer T (NKT) cells and CD4⁺CD25⁺ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance. Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4⁺CD25⁺ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain. We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4⁺CD25⁺ Treg cells decrease in an age-dependent manner. We show that treatment with α-galactosylceramide increases the size of the CD4⁺CD25⁺ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4⁺CD25⁺ Treg cells to inhibit proliferation of CD4⁺CD25⁻ T cells. Our data indicate that NKT cells and CD4⁺CD25⁺ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with α-galactosylceramide. Induced cooperation of NKT cells and CD4⁺CD25⁺ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes.

Keywords: invariant NKT cell; Treg; Foxp3; type 1 diabetes; α-galactosylceramide

Document Type: Research article

DOI: 10.1111/j.1745-7270.2008.00410.x

Affiliations: 1: Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

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Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with α-galactosylceramide

Cooperation of invariant NKT cells and CD4⁺CD25⁺ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with α-galactosylceramide