Gene therapy for management of lupus: Correction of Fas and Fas ligand-induced apoptosis in murine disease — therapeutic rationale and ... View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2000

AUTHORS

Huang-Ge Zhang , Martin Fleck , Hui-Chen Hsu , Carl K. Edwards , David T. Curiel , Tong Zhou , John D. Mountz

ABSTRACT

Identification of mutations of fas and fas ligand (fasL) in murine models of autoimmune disease have provided an important experimental tools for the analysis of tolerance and autoimmune disease. Mutations of fasL and fas 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 systemic lupus erythematosus (SLE) [6]. Furthermore, accumulating evidence suggests that dysregulation of apoptosis or altered levels of expression of FasL and Fas play 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. In this chapter, we shall describe potential applications of gene therapy to develop strategies to overcome these defects. More... »

PAGES

95-117

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-0348-8478-5_7

DOI

http://dx.doi.org/10.1007/978-3-0348-8478-5_7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1033693387


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