期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 104, 期 8, 页码 2821-2826出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0611646104
关键词
antigen-presenting cells; autoimmunity; type 1 diabetes; nonobese diabetic (NOD) mice
资金
- NIAID NIH HHS [AI 51573, P01 AI051573] Funding Source: Medline
- NIDDK NIH HHS [5K01 DK 071586-02, K08 DK070029, 1K08 DK 070029-01, K01 DK071586, R21 DK 60186] Funding Source: Medline
CD4(+)CD25(+)Foxp3(+) regulatory T cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natural) or differentiated in the periphery outside the thymus (induced). Here we show that beta-cell peptide-pulsed dendritic cells (DCs) from nonobese diabetic (NOD) mice can effectively induce CD4(+)CD25(+)Foxp3(+) T cells from naive islet-specific CD4(+)CD25(-) T cells in the presence of TGF-beta 1. These induced, antigen-specific T regs maintain high levels of clonotype-specific T cell receptor expression and exert islet-specific suppression in vitro. When cotransferred with diabetogenic cells into NOD scid recipients, T regs induced with DCs and TGF-beta 1 prevent the development of diabetes. Furthermore, in overtly NOD mice, these cells are able to significantly protect syngeneic islet grafts from established destructive autoimmunity. These results indicate a role for DCs in the induction of antigen-specific CD4(+)CD25(+)Foxp3(+) T cells that can inhibit fully developed autoimmunity in a nonlymphopoenic host, providing an important potential strategy for immunotherapy in patients with autoimmune diabetes.
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