期刊
NATURE IMMUNOLOGY
卷 6, 期 8, 页码 785-792出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1220
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- NIAID NIH HHS [T32 AI007290, T32 AI07290, T32 AI007244] Funding Source: Medline
- NIDDK NIH HHS [R21 DK061329, DK61329] Funding Source: Medline
- NIGMS NIH HHS [GM039476, R01 GM039476, GM065230, R01 GM065230] Funding Source: Medline
- NIMH NIH HHS [P30MH62261, P30 MH062261] Funding Source: Medline
It is unclear if the interaction between CD8 and the T cell receptor (TCR)-CD3 complex is constitutive or antigen induced. Here, fluorescence resonance energy transfer microscopy between fluorescent chimeras of CD3 zeta and CD8 beta showed that this interaction was induced by antigen recognition in the immunological synapse. Nonstimulatory endogenous or exogenous peptides presented simultaneously with antigenic peptides increased the CD8-TCR interaction. This finding indicates that the interaction between the intracellular regions of a TCR-CD3 complex recognizing its cognate peptide-major histocompatibility complex (MHC) antigen, and CD8 ( plus the kinase Lck), is enhanced by a noncognate CD8-MHC interaction. Thus, the interaction of CD8 with a nonstimulatory peptide-MHC complex helps mediate T cell recognition of antigen, improving the coreceptor function of CD8.
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