期刊
JOURNAL OF IMMUNOLOGY
卷 174, 期 1, 页码 80-89出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.1.80
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- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI029544, R37AI029544] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI 29544] Funding Source: Medline
The transfer of membrane proteins from APC to T cells was initially described in the 1970s, and subsequent work has described two mechanisms of transfer: APC-derived exosomes and direct transfer of small packets, while cells remain conjugated. Using fibroblast APC expressing a GFP-tagged I-E-k Molecule with covalently attached antigenic peptide, we observed a third mechanism in live cell imaging: T cells spontaneously dissociating from APC often capture MHC:peptide complexes directly from the immunological synapse. Using two I-E-k-restricted murine TCR transgenic T cells with different peptide specificity, we show in this study that the MHC transfer is peptide specific. Using blocking Abs, we found that MHC:peptide transfer in this system requires direct TCR-MHC:peptide interactions and is augmented by costimulation through CD28-CD80 interactions. Capture of the GFP-tagged MHC:peptide complexes correlates with an activated phenotype of the T cell, elevated CD69 with down-modulated TCR. The transferred MHC:peptide molecules transferred to the T cell are associated with molecules that imply continued TCR signaling; p56(lck), phosphotyrosine, and polarization of the actin cytoskeleton.
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