Autoimmunity Due to Defective NUR77, Fas, and TNF-RI Apoptosis View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1996

AUTHORS

John D. Mountz , Carl K. Edwards , Jianhua Cheng , Pingar Yang , Zheng Wang , Changdan Liu , Xiao Su , Horst Bluethmann , Tong Zhou

ABSTRACT

Several molecules and pathways known to be of importance in apoptosis have been described in the thymus; however, their contribution to clonal deletion and tolerance induction remains controversial1–4. Although knockout of p53 leads to decreased sensitivity of murine thymocytes to radiation-induced apoptosis, negative selection remains intact5–7. Fas is a cell surface receptor that mediates apoptosis by interaction with a specific ligand and is expressed on most murine thymocytes8–11. Although mutant Fas antigen and Fas ligand cause autoimmune disease in 1pr/lpr and gld/gld mice, respectively10–12 no major negative selection defects have been found in Ipr/lpr mice13–17. Therefore, it is unlikely that Fas antigen is directly involved in negative selection in the thymus, but may be involved in apoptosis during early T cell development in the thymus. We have previously proposed that Fas expression duirng early thymocyte development plays a role in positive selection or pre-positive selection of thymocytes (Figure 1). More... »

PAGES

241-262

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4899-0274-0_25

DOI

http://dx.doi.org/10.1007/978-1-4899-0274-0_25

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1005929117

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8910690


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