Contributions
Abstract: EP1461
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models
Background: Neuromyelitis optica (NMO) also known as Devic´s disease is a central nervous system (CNS) autoimmune disease that preferentially affects the spinal cord and optic nerve. The disease is mediated by autoantibodies against Aquaporin 4 (AQP4). Myasthenia gravis (MG) is also an antibody-mediated disease that affects the neuromuscular junction, caused by autoantibodies against the nicotinic acetylcholine receptor (AChR) in 85% of patients. Recently increased prevalence of NMO was found in patients with MG and vice versa.
Currently the experimental autoimmune MG (EAMG) murine model is a good model for MG, but there is no good model for NMO.
Aims: To verify whether passive and active immunization with NMO-Ig and AQP4 peptides respectively, affect the severity and/or induce CNS pathology in EAMG.
Methods: We used EAMG induced in C57bl mice by immunization with Torpedo AChR and subjected the animals to passive transfer of NMO-IgG or to immunization with AQP4-derived peptide.
Results: Injection of either AQP4 peptide or NMO-Ig to EAMG or to naïve mice caused increased fatigability and aggravation of EAMG symptoms as expressed by augmented muscle weakness (but not paralysis), decremental response to repetitive nerve stimulation, increased neuromuscular jitter, and aberration of immune responses.
Conclusions: Increased disease severity in EAMG mice following immunization with the NMO autoantigen AQP4 or by NMO-Ig mediated by augmented inflammatory response can explain the clinical observation of increased susceptibility of patients with one autoimmune disease to develop a second autoimmune syndrome. Those models can serve as a tool to advance our understanding of how autoimmunity progresses and could help tailor therapy for those patients.
Disclosure:
Brill L: nothing to disclose
Mizrachi T: nothing to disclose
Rabi M: nothing to disclose
Nevo Y: nothing to disclose
Fellig Y: nothing to disclose
Zur M: nothing to disclose
Karussis D: nothing to disclose
Abramsky O: nothing to disclose
Brenner T: nothing to disclose
Vaknin Dembinsky A: nothing to disclose
Abstract: EP1461
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models
Background: Neuromyelitis optica (NMO) also known as Devic´s disease is a central nervous system (CNS) autoimmune disease that preferentially affects the spinal cord and optic nerve. The disease is mediated by autoantibodies against Aquaporin 4 (AQP4). Myasthenia gravis (MG) is also an antibody-mediated disease that affects the neuromuscular junction, caused by autoantibodies against the nicotinic acetylcholine receptor (AChR) in 85% of patients. Recently increased prevalence of NMO was found in patients with MG and vice versa.
Currently the experimental autoimmune MG (EAMG) murine model is a good model for MG, but there is no good model for NMO.
Aims: To verify whether passive and active immunization with NMO-Ig and AQP4 peptides respectively, affect the severity and/or induce CNS pathology in EAMG.
Methods: We used EAMG induced in C57bl mice by immunization with Torpedo AChR and subjected the animals to passive transfer of NMO-IgG or to immunization with AQP4-derived peptide.
Results: Injection of either AQP4 peptide or NMO-Ig to EAMG or to naïve mice caused increased fatigability and aggravation of EAMG symptoms as expressed by augmented muscle weakness (but not paralysis), decremental response to repetitive nerve stimulation, increased neuromuscular jitter, and aberration of immune responses.
Conclusions: Increased disease severity in EAMG mice following immunization with the NMO autoantigen AQP4 or by NMO-Ig mediated by augmented inflammatory response can explain the clinical observation of increased susceptibility of patients with one autoimmune disease to develop a second autoimmune syndrome. Those models can serve as a tool to advance our understanding of how autoimmunity progresses and could help tailor therapy for those patients.
Disclosure:
Brill L: nothing to disclose
Mizrachi T: nothing to disclose
Rabi M: nothing to disclose
Nevo Y: nothing to disclose
Fellig Y: nothing to disclose
Zur M: nothing to disclose
Karussis D: nothing to disclose
Abramsky O: nothing to disclose
Brenner T: nothing to disclose
Vaknin Dembinsky A: nothing to disclose