Nature Immunology 7, 83 - 92 (2005)
Published online: 27 November 2005; | doi:10.1038/ni1289
Visualizing regulatory T cell control of autoimmune responses in nonobese diabetic miceQizhi Tang1, 2, Jason Y Adams1, Aaron J Tooley2, Mingying Bi1, Brian T Fife1, Pau Serra4, Pere Santamaria4, Richard M Locksley3, Matthew F Krummel2, 5
& Jeffrey A Bluestone1, 2, 51
University of California, San Francisco, Diabetes Center, Department of Medicine, University of California, San Francisco, California 94143, USA. 2
Department of Pathology, University of California, San Francisco, California 94143, USA. 3
Howard Hughes Medical Institute and Department of Medicine, University of California, San Francisco, California 94143, USA. 4
Julia McFarlane Diabetes Research Centre and Department of Microbiology & Infectious Diseases, University of Calgary, Calgary, Alberta T2N 4N1, Canada. 5
These authors contributed equally to this work.
Correspondence should be addressed to Jeffrey A Bluestone jbluest@diabetes.ucsf.edu The in vivo mechanism of regulatory T cell (Treg cell) function in controlling autoimmunity remains controversial. Here we have used two-photon laser-scanning microscopy to analyze lymph node priming of diabetogenic T cells and to delineate the mechanisms of Treg cell control of autoimmunity in vivo. Islet antigen–specific CD4+CD25- T helper cells (TH cells) and Treg cells swarmed and arrested in the presence of autoantigens. These TH cell activities were progressively inhibited in the presence of increasing numbers of Treg cells. There were no detectable stable associations between Treg and TH cells during active suppression. In contrast, Treg cells directly interacted with dendritic cells bearing islet antigen. Such persistent Treg cell–dendritic cell contacts preceded the inhibition of TH cell activation by dendritic cells, supporting the idea that dendritic cells are central to Treg cell function in vivo.
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