Apoptosis-induced inhibition of CD1d-mediated antigen presentation: different roles for caspases and signal transduction pathways
Authors
Khan, Masood A.Sriram, Venkataraman
Renukaradhya, Gourapura J.
Du, Wenjun
Gervay-Hague, Jacquelyn
Brutkiewicz, Randy R.
UMass Chan Affiliations
Department of Microbiology and ImmunologyGraduate School of Biomedical Sciences
Document Type
Journal ArticlePublication Date
2008-03-19Keywords
Animals; Antigen Presentation; Antigens, CD1; Antigens, CD1d; Apoptosis; Camptothecin; Caspases; Cells, Cultured; Ceramides; Coculture Techniques; Female; Galactosylceramides; Meperidine; Mice; Mice, Inbred C57BL; Protein Kinase C-delta; Signal Transduction; p38 Mitogen-Activated Protein KinasesLife Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
The stimulation of programmed cell death can either enhance or inhibit antigen presentation by classic major histocompatibility complex molecules. In the current study, we report that the induction of apoptosis by topoisomerase I inhibition or elevation of intracellular ceramide levels substantially impairs CD1d-mediated antigen presentation. In the former case, such a reduction occurred via the regulation of both the p38 mitogen-activated protein kinases and protein kinase C delta signal transduction pathways as well as the caspase cascade, whereas the latter was p38-(but not caspase)-dependent. Confocal microscopic analysis showed an altered intracellular distribution of CD1d following the inhibition topoisomerase I or by an increase in intracellular ceramide levels, that was prevented by p38 and caspase inhibitors. Thus, the induction of apoptosis in antigen presenting cells severely compromises CD1d-mediated antigen presentation by multiple mechanisms.Source
Immunology. 2008 Sep;125(1):80-90. Epub 2008 Mar 14. Link to article on publisher's siteDOI
10.1111/j.1365-2567.2008.02823.xPermanent Link to this Item
http://hdl.handle.net/20.500.14038/32914PubMed ID
18346153Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1111/j.1365-2567.2008.02823.x