Cargando…
Complement regulator CD59 prevents peripheral organ injury in rats made seropositive for neuromyelitis optica immunoglobulin G
Pathogenesis in aquaporin-4 immunoglobulin G (AQP4-IgG) seropositive neuromyelitis optica spectrum disorders (herein called NMO) involves complement-dependent cytotoxicity initiated by AQP4-IgG binding to astrocyte AQP4. We recently reported that rats lacking complement inhibitor protein CD59 were h...
Autores principales: | Yao, Xiaoming, Verkman, Alan S. |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5532786/ https://www.ncbi.nlm.nih.gov/pubmed/28750658 http://dx.doi.org/10.1186/s40478-017-0462-4 |
Ejemplares similares
-
Marked central nervous system pathology in CD59 knockout rats following passive transfer of Neuromyelitis optica immunoglobulin G
por: Yao, Xiaoming, et al.
Publicado: (2017) -
Complement-dependent bystander injury to neurons in AQP4-IgG seropositive neuromyelitis optica
por: Duan, Tianjiao, et al.
Publicado: (2018) -
Complement-independent retinal pathology produced by intravitreal injection of neuromyelitis optica immunoglobulin G
por: Felix, Christian M., et al.
Publicado: (2016) -
The evolving mystery of why skeletal muscle is spared in seropositive neuromyelitis optica
por: Verkman, Alan S., et al.
Publicado: (2018) -
Complement-independent bystander injury in AQP4-IgG seropositive neuromyelitis optica produced by antibody-dependent cellular cytotoxicity
por: Duan, Tianjiao, et al.
Publicado: (2019)