Management of Murine Lupus by Correction of Fas and Fas Ligand-Induced Apoptosis View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1999

AUTHORS

Hui-Chen Hsu , Huang-Ge Zhang , Tong Zhou , John D. Mountz

ABSTRACT

Identification of mutations of fas and fas ligand (fasL) genes in murine models of autoimmune disease has provided an important experimental tool for the analysis of tolerance and autoimmune disease. Mutations of fasL and fas genes are not a common cause of autoimmune disease in humans, although a mutation of the fas gene has been associated with autoimmune lymphoproliferative syndrome (1–5), and we have described a mutation of the fasL gene in one patient with SLE (6). Furthermore, accumulating evidence suggests that dysregulation of apoptosis or altered levels of expression of FasL and Fas plays an important role in the pathogenesis of diseases associated with immune regulation (6–11). Fas apoptosis appears to be the primary mechanism for elimination of autoreactive T cells outside the thymus. FasL regulation is tightly controlled, and specific cells and transcription factors have been identified that play a role in this process. Further investigations of Fas/FasL regulation should allow development of strategies to restore T-cell tolerance in autoimmune situations. The first part of this chapter uses Fas/FasL as an example to demonstrate the importance of apoptosis in the regulation of immune homeostasis. The second part of this chapter follows the footsteps of investigators in this field to understand how one can apply modern technology to understand mechanisms associated with genetic defect-related autoimmune disease and to develop strategies to overcome these defects. More... »

PAGES

671-693

Book

TITLE

Lupus

ISBN

978-1-4757-5686-9
978-1-59259-703-1

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-59259-703-1_40

DOI

http://dx.doi.org/10.1007/978-1-59259-703-1_40

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1038580972


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