Glycosylphosphatidylinositol-anchored H-2D(b) molecules are defective in antigen processing and presentation to cytotoxic T lymphocytes

被引:9
|
作者
Cariappa, A
Flyer, DC
Rollins, CT
Roopenian, DC
Flavell, RA
Brown, D
Waneck, GL
机构
[1] MASSACHUSETTS GEN HOSP,DEPT SURG,CHARLESTOWN,MA 02129
[2] HARVARD UNIV,SCH MED,DEPT PATHOL,CHARLESTOWN,MA
[3] MASSACHUSETTS GEN HOSP,DEPT PATHOL,CHARLESTOWN,MA 02129
[4] PENN STATE UNIV,COLL MED,DEPT MICROBIOL & IMMUNOL,HERSHEY,PA
[5] JACKSON LAB,BAR HARBOR,ME 04609
[6] YALE UNIV,SCH MED,IMMUNOBIOL SECT,NEW HAVEN,CT 06510
[7] YALE UNIV,SCH MED,HOWARD HUGHES MED INST,NEW HAVEN,CT 06510
关键词
glycosylphosphatidylinositol anchor; major histocompatibility antigen class I; antigen processing; cytotoxic T lymphocyte recognition;
D O I
10.1002/eji.1830260938
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Glycosylphosphatidylinositol-anchored (GPI)-D-b molecules are defective in mediating cytotoxic T lymphocytes (CTL) lysis of transfected lymphoma cells, compared to their transmembrane (TM) counterpart. This defect is manifest when antigenic peptide must be processed and presented through the endogenous pathway. These same transfectants can be lysed by allospecific CTL, or by antigen-specific D-b-restricted CTL when pulsed with appropriate exogenous synthetic peptide, demonstrating that they can bind and present peptide for CTL-mediated lympholysis. The defect apparently results from differences between GPI-D-b and TM-D-b assembly and transport, or from differences in membrane topology that affect CD8+ Cn recognition of major histocompatibility complex/peptide complex.
引用
收藏
页码:2215 / 2224
页数:10
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