title: If pemphigus vulgaris IgG are the cause of acantholysis, new IgG-independent mechanisms are the concause.
abstract: Pemphigus vulgaris (PV) is a disease of epidermal adhesion. Its pathogenesis is currently traced back to the action of autoantibodies against antigens located within the intercellular substance of keratinocytes, such as desmogleins and acetylcholine receptors. In the present paper, we sought to elucidate the non-IgG-mediated effects of PV sera on keratinocytes. Results showed that PV sera depleted of IgG were able to induce well-defined changes on keratinocyte morphology and metabolic activity. Indeed, PV IgG-free sera determined marked alterations on cell shape, accompanied by partial loss of keratinocyte-keratinocyte interactions within 48 h after treatment. Furthermore, PV IgG-depleted sera caused a sharp reduction of cell viability along with a less sustained weakening of intercellular adhesion strength. In light of the above findings, loss of cell-cell adhesion in PV occurs as a result of the cooperating action of both IgG and non-IgG-mediated mechanisms. These data have remarkable consequences on experimental models of PV and might open new "biological" approaches to its therapy. Thus, researchers are well advised that PV pathophysiology cannot be faithfully reproduced by leaving non-IgG serum factors out of consideration.
authors.affiliation: Regional Center on Craniofacial Malformations-MRI, 1st School of Medicine and Surgery, II University of Naples, Naples, Italy. cirillo.sun@libero.it
authors.forename: Nicola
authors.initials: N
authors.lastname: Cirillo
authors.forename: Michele
authors.initials: M
authors.lastname: Lanza
authors.forename: Felice
authors.initials: F
authors.lastname: Femiano
authors.forename: Giovanni Maria
authors.initials: GM
authors.lastname: Gaeta
authors.forename: Alfredo
authors.initials: A
authors.lastname: De Rosa
authors.forename: Fernando
authors.initials: F
authors.lastname: Gombos
authors.forename: Alessandro
authors.initials: A
authors.lastname: Lanza
mesh_terms: D000051:Acantholysis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D001323:Autoantibodies / Q000097:blood*; D016022:Case-Control Studies; D002448:Cell Adhesion; D002460:Cell Line; D048430:Cell Shape; D002470:Cell Survival; D051184:Desmoglein 3 / Q000378:metabolism; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007365:Intercellular Junctions; D015603:Keratinocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D010392:Pemphigus / Q000150:complications* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D044967:Serum / Q000276:immunology / Q000378:metabolism*
chemical_list: D001323:Autoantibodies; C071894:DSG3 protein, human; D051184:Desmoglein 3; D007074:Immunoglobulin G