Tapasin decreases immune responsiveness to a model tumor antigen

被引:11
作者
Turnquist, HR
Kohlgraf, KG
McIlhaney, MM
Mosley, RL
Hollingsworth, MA
Solheim, JC
机构
[1] Univ Nebraska, Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA
[2] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA
[3] Univ Nebraska, Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA
关键词
tapasin; MHC; tumor antigen; antigen presentation; pancreatic cancer;
D O I
10.1023/B:JOCI.0000029118.51587.d9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The T-cell response against cancer is dependent on the cell surface presentation of tumor-associated or tumor-specific peptides by major histocompatibility complex (MHC) class I molecules. We found that tapasin, a chaperone protein that normally assists in the assembly of MHC class I molecules, is undetectable in an unstimulated pancreatic tumor cell line, Panc02, and only very weakly expressed after gamma-interferon stimulation. Transfection of tapasin into the Panc02 cells did not quantitatively increase MHC class I surface expression or detectably affect MHC class I association with peptide and beta(2)-microglubulin (beta(2)m). However, we found that transfected tapasin downregulated immune reactivity against a model tumor antigen, MUC1. Although tapasin has been previously shown by others to increase immune recognition of particular antigens, our results suggest that tapasin has a negative impact on the presentation of an immunodominant epitope from a specific model tumor antigen.
引用
收藏
页码:462 / 470
页数:9
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