Abstract
The autoimmune, blistering disease pemphigus vulgaris is caused by autoantibodies against the desmosomal cadherins, mainly desmoglein-3. Recently, it has been shown that blocking the neonatal Fc receptor (FcRn) can lead to a rapid decrease of pathogenic IgG and an improvement of various autoimmune diseases, including pemphigus, myasthenia gravis and autoimmune thrombocytopenia. Binding of IgG type antibodies to FcRn results in antibody recycling and increases the plasma half-life of pathogenic autoantibodies, contributing to disease phenotype.
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