期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 207, 期 9, 页码 1891-1905出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20092627
关键词
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资金
- Swiss National Science Foundation [3100A0-105895, 310030-127042]
- Geneva Cancer League
- Swiss Multiple Sclerosis Society
- National Center of Competence in Research on Neural Plasticity and Repair (NCCR-NEURO)
- EU
- European Molecular Biology Organization
- Roche
- Novartis Research Foundations
- Institut National de la Sante et de la Recherche Medicale
- Faculty of Medicine at the University of Geneva
- Swiss National Science Foundation
Although plasmacytoid dendritic cells (pDCs) express major histocompatibility complex class II (MHCII) molecules, and can capture, process, and present antigens (Ags), direct demonstrations that they function as professional Ag-presenting cells (APCs) in vivo during ongoing immune responses remain lacking. We demonstrate that mice exhibiting a selective abrogation of MHCII expression by pDCs develop exacerbated experimental autoimmune encephalomyelitis (EAE) as a consequence of enhanced priming of encephalitogenic CD4(+) T cell responses in secondary lymphoid tissues. After EAE induction, pDCs are recruited to lymph nodes and establish MHCII-dependent myelin-Ag-specific contacts with CD4(+) T cells. These interactions promote the selective expansion of myelin-Ag-specific natural regulatory T cells that dampen the autoimmune T cell response. pDCs thus function as APCs during the course of EAE and confer a natural protection against autoimmune disease development that is mediated directly by their ability to present of Ags to CD4(+) T cells in vivo.
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