We performed partial evaluation of pemphigus vulgaris (PV) autoantibody profile 
using the protein array technology. The sera from seven patients with acute PV 
and five healthy donors were probed for the presence of autoantibodies 
characteristic of the organ-non-specific autoimmune disorders rheumatoid 
arthritis, lupus erythematosus, scleroderma, diabetes and some other autoimmune 
disorders, but not to desmosomal proteins. The array targeted 785 human genes 
amplified using Mammalian Gene Clone Collection with gene-specific primers 
containing 20-bp nucleotide extension complementary to ends of linear pXT7 
vector. The array identified PV antibodies significantly (P<0.05) differentially 
reactive with 16 antigens, most of which were cell-surface proteins, such as 
CD2, CD31, CD33, CD36, CD37, CD40, CD54, CD66c and CD84 molecules, 
nicotinamide/nicotinic acid mononucleotide adenylyltransferase, immunoglobulin 
heavy chain constant region gamma 2 and others. Reactivity with Fc-IgG helps 
explain an ability of the chimeric desmoglein constructs to absorb out all 
disease-causing PV antibodies. Anti-M(1) muscarinic receptor antibody was also 
identified, consistent with the facts that while blockade of this receptor 
causes keratinocyte detachment, its activation is therapeutic in PV. Further 
proteomics analysis of PV antibodies should help elucidate the immunopathogenic 
mechanisms underlying keratinocyte detachment and blistering.