期刊
NATURE IMMUNOLOGY
卷 7, 期 1, 页码 83-92出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1289
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- NIAID NIH HHS [AI30663, R21 AI066097-01, R01 AI030663, R37 AI46643, R21 AI066097-02, R37 AI046643, R21 AI066097] Funding Source: Medline
- NIDDK NIH HHS [P30 DK063720] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R21AI066097, R01AI030663, R37AI046643] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK063720] Funding Source: NIH RePORTER
The in vivo mechanism of regulatory T cell (T-reg 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 T-reg cell control of autoimmunity in vivo. Islet antigen-specific CD4(+)CD25(-) T helper cells (T-H cells) and T-reg cells swarmed and arrested in the presence of autoantigens. These T-H cell activities were progressively inhibited in the presence of increasing numbers of T-reg cells. There were no detectable stable associations between T-reg and T-H cells during active suppression. In contrast, T-reg cells directly interacted with dendritic cells bearing islet antigen. Such persistent T-reg cell-dendritic cell contacts preceded the inhibition of T-H cell activation by dendritic cells, supporting the idea that dendritic cells are central to T-reg cell function in vivo.
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