期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 205, 期 11, 页码 2561-2574出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20081212
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资金
- Swiss National Science Foundation [31-63885, 31-109832]
- European Commission FP6 Network of Excellence [LSHG-CT-2003-502935 MAIN, LSHB-CT-2004-512074 DC-THERA, LSHG-CT-2005-005203 MUGEN]
- Helmut Horten Foundation
- Boehringer Ingelheim Fonds
- European Union-funded International Graduate Program in Molecular Medicine
There is growing evidence that the maturation state of dendritic cells (DCs) is a critical parameter determining the balance between tolerance and immunity. We report that mouse CD4(+) effector memory T (T-EM) cells, but not naive or central memory T cells, constitutively expressed CD40L at levels sufficient to induce DC maturation in vitro and in vivo in the absence of antigenic stimulation. CD4(+) T-EM cells were excluded from resting lymph nodes but migrated in a CD62P-dependent fashion into reactive lymph nodes that were induced to express CD62P, in a transient or sustained fashion, on high endothelial venules. Trafficking of CD4(+) T-EM cells into chronic reactive lymph nodes maintained resident DCs in a mature state and promoted naive T cell responses and experimental autoimmune encephalomyelitis (EAE) to antigens administered in the absence of adjuvants. Antibodies to CD62P, which blocked CD4(+) T-EM cell migration into reactive lymph nodes, inhibited DC maturation, T cell priming, and induction of EAE. These results show that T EM cells can behave as endogenous adjuvants and suggest a mechanistic link between lymphocyte traffic in lymph nodes and induction of autoimmunity.
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