6533b854fe1ef96bd12ae938

RESEARCH PRODUCT

Autoantibody depletion ameliorates disease in murine experimental autoimmune encephalomyelitis.

Pankaj BansalTarique KhanUta BussmeyerE. Sally WardHéctor Perez MontoyoRaimund J. OberDilip K. Challa

subject

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisShort CommunicationImmunologyCentral nervous systemCHO CellsReceptors FcBiologyProtein EngineeringImmunoglobulin GAntibodiesMyelin oligodendrocyte glycoproteinPathogenesisMiceCricetulusCricetinaemedicineImmunology and AllergyAnimalsHumansAutoantibodiesMultiple sclerosisExperimental autoimmune encephalomyelitisHistocompatibility Antigens Class IAutoantibodymedicine.diseaseRecombinant ProteinsMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GImmunologybiology.proteinFemaleMyelin-Oligodendrocyte GlycoproteinAntibodyProtein Binding

description

Much data support a role for central nervous system antigen-specific antibodies in the pathogenesis of multiple sclerosis (MS). The effects of inducing a decrease in (auto)antibody levels on MS or experimental autoimmune encephalomyelitis (EAE) through specific blockade of FcRn, however, remain unexplored. We recently developed engineered antibodies that lower endogenous IgG levels by competing for binding to FcRn. These Abdegs ("antibodies that enhance IgG degradation") can be used to directly assess the effect of decreased antibody levels in inflammatory diseases. In the current study, we show that Abdeg delivery ameliorates disease in an EAE model that is antibody dependent. Abdegs could therefore have promise as therapeutic agents for MS.

yearjournalcountryeditionlanguage
2013-09-01mAbs
10.4161/mabs.25439https://pubmed.ncbi.nlm.nih.gov/23846320