Role of membrane complement regulators in XXXX .

@entity1 @entity1009 @entity1652 @entity806 @entity3951 @entity9819
BACKGROUND: It is unclear why @entity3951 -IgG primarily causes central nervous system lesions by activating complement, but generally spares peripheral @entity3951 -expressing organs. OBJECTIVES: To determine whether peripheral @entity3951 -expressing cells are protected from complement-mediated damage by expressing complement regulators. METHODS: @entity1 tissue and cultured @entity1 cells were immunostained for @entity3951 ( @entity3951 ), @entity806 , @entity9819 and @entity1009 . We also determined the vulnerability to @entity3951 -IgG and complement-mediated damage of astrocytes cultured alone or co-cultured with endothelial cells. RESULTS: In normal brain, astrocyte end-feet express @entity3951 , but are devoid of @entity806 , @entity9819 and @entity1009 . Immunoreactivity for @entity806 , @entity9819 and @entity1009 is not increased in or around @entity1652 lesions. In kidney @entity3951 is co-expressed with @entity806 and @entity9819 , in stomach @entity3951 is co-expressed with @entity806 and in skeletal muscle @entity3951 is co-expressed with @entity806 . Astrocytes cultured alone co-express @entity3951 and @entity1009 but, in astrocyte-endothelial co-cultures, @entity3951 is found in cell processes devoid of @entity1009 . Astrocytes co-cultured with endothelial cells are more vulnerable to @entity3951 -IgG and complement-mediated lysis than astrocytes cultured alone. CONCLUSIONS: Complement regulators protect peripheral organs, but not the central nervous system, from @entity3951 -IgG and complement-mediated damage. Our findings may explain why @entity1652 primarily damages the central nervous system, but spares peripheral organs.
