Molecular analysis of decay accelerating factor as a potential susceptibility factor to developing treatment resistant extraocular muscle involvement in Myasthenia Gravis

Myasthenia gravis (MG) is an autoimmune disorder in which auto-antibodies directed at the acetylcholine receptors (AChR) of the neuromuscular junction (NMJ) block, alter or destroy their targets. The anti-AChR antibodies cause activation of the classical complement pathway leading to inflammatory injury at the NMJ. Decay Accelerating Factor (DAF), a member of complement regulatory proteins, prevents activation of autologous components of complement pathways. The absence of DAF, in knock-out mouse models, has been shown to significantly increase the susceptibility to experimental autoimmune MG. A previous study showed that a high proportion of South African MG patients of African genetic ancestry develop immunosuppressive therapyresistant extraocular muscle (EOM) dysfunction. We hypothesized that these patients have deficient DAF expression in their EOMs resulting in less protection from complement injury.

Grantor dc:publisher.institution

Department of Human Biology

Year dc:date.issued

2009

Author dc:creator

• Uwimpuhwe, Henriette

Advisors dc:contributor.advisor

• Heckmann, Jeannine
• Ballo, Robea
• Prince, Sharon

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/11427/3208

OAI identifier oai:identifier

oai:open.uct.ac.za:11427/3208