期刊
TRAFFIC
卷 3, 期 5, 页码 358-366出版社
BLACKWELL MUNKSGAARD
DOI: 10.1034/j.1600-0854.2002.30505.x
关键词
CD1; cross-presentation; dendritic cell; gp96; GRP94; macrophage; MHC class I
类别
资金
- NCI NIH HHS [1F32CA9016901] Funding Source: Medline
- NIDDK NIH HHS [DK53058] Funding Source: Medline
GRP94 (gp96)-associated peptides can elicit cellular Immune responses, an activity thought to reflect the presence of a cell surface receptor (CD91) on antigen-presenting cells that mediates GRP94 internalization and trafficking to an amenable site for peptide transfer to major histocompatibility complex class I molecules. We report that GRP94 internalized by receptor-mediated endocytosis is trafficked to a Rab5a, CD1 and transferrin-negative, Fc receptor and major histocompatibility complex class I-positive endocytic compartment. Receptor-internalized GRP94 did not access the endoplasmic reticulum of antigen-presenting cells. To Identify the site of re-presentation of GRP94-associated peptides, kinetic analyses were performed utilizing GRP94-OVA (SIINFEKL) peptide complexes, with peptide re-presentation assayed with the K-b-SIINFEKL-specific MAb, 25-D1.16. Analyses of the kinetics of re-presentation of GRP94-associated peptides, under conditions in which de novo synthesis of major histocompatibility complex class I molecules was inhibited, identified a post-endoplasmic reticulum compartment, accessed by mature major histocompatibility complex class 1, as the predominant site of GRP94-associated peptide exchange onto major histocompatibility complex class I.
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