CD43 cross-linking increases the Fas-induced apoptosis through induction of Fas aggregation in Jurkat T-cells.
- Author:
Hae Jung KIM
1
;
Hyo Jin PARK
;
Weon Seo PARK
;
Youngmee BAE
Author Information
1. Division of Specific Organ Cancer, Research Institute National Cancer Center, Goyang 411-769, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
apoptosis;
antigens, CD43;
antigens, CD95;
caspase;
Jurkat cells;
T-lymphocytes
- MeSH:
Receptor Aggregation/immunology;
Jurkat Cells;
Humans;
Caspases/metabolism;
Apoptosis/*immunology;
Antigens, Surface/metabolism;
Antigens, CD95/metabolism/*physiology;
Antigens, CD43/metabolism/*physiology;
Antibodies, Monoclonal/metabolism
- From:Experimental & Molecular Medicine
2006;38(4):357-363
- CountryRepublic of Korea
- Language:English
-
Abstract:
CD43 (sialophorin, leukosialin) is a heavily sialylated surface protein expressed on most leukocytes and platelets including T cells. Although CD43 antigen is known to have multiple and complex structure, exact function of CD43 in each cell type is not completely understood. Here we evaluated the role of CD43 in Fas (CD95)-induced cell death in human T lymphoblastoid cell line, Jurkat. Crosslinking CD43 antigen by K06 mAb increased the Fas-mediated Jurkat cell apoptosis and the augmentation was inhibited by treatment with caspase inhibitors. Further, CD43 signaling of Jurkat cells induced Fas oligomerization on the cell surfaces implying that CD43 ligation have effects on early stage of Fas-induced T cell death. These also suggest that CD43 might play an important role in contraction of the immune response by promotion of Fas-induced apoptosis in human T cells.
