2020
DOI: 10.1016/j.intimp.2019.106149
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Mechanisms of synergy of autoantibodies to M3 muscarinic acetylcholine receptor and secretory pathway Ca2+/Mn2+-ATPase isoform 1 in patients with non-desmoglein pemphigus vulgaris

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Cited by 12 publications
(22 citation statements)
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“…Furthermore, the acantholytic activity of pre-absorbed PV IgGs can be restored by adding the eluted AuAbs [47]. Similar results were observed in the in vitro models of PVthe neonatal mouse skin explant and the 3D organ culture of human epidermis [46,47]. However, when given alone, neither of these AuAbs induce acantholysis on their own, suggesting that a simultaneous hit by a pool of non-Dsg AuAbs to different self-antigens is required to disrupt the integrity of epidermis.…”
Section: Non-desmoglein Pemphigussupporting
confidence: 68%
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“…Furthermore, the acantholytic activity of pre-absorbed PV IgGs can be restored by adding the eluted AuAbs [47]. Similar results were observed in the in vitro models of PVthe neonatal mouse skin explant and the 3D organ culture of human epidermis [46,47]. However, when given alone, neither of these AuAbs induce acantholysis on their own, suggesting that a simultaneous hit by a pool of non-Dsg AuAbs to different self-antigens is required to disrupt the integrity of epidermis.…”
Section: Non-desmoglein Pemphigussupporting
confidence: 68%
“…On average, 10-15% of acute PV patients are negative for anti-Dsg1/3 AuAbs [39][40][41][42][43][44][45]. Since the immunopathologic mechanisms of acantholysis in these PV patients may be different, such "non-Dsg PV" (the term coined by Chernyavsky et al [46]) is considered to be atypical. Thus far, the best studied self-antigens in non-Dsg PV are Dsc3, M3AR and SPCA1 [47].…”
Section: Non-desmoglein Pemphigusmentioning
confidence: 99%
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“…The pemphigoid group is now known to include at least eight disorders for which the molecular target antigens have been identified [4], although controversy exists regarding the pathogenic mechanisms of blistering [5]. In pemphigus, distinct autoantibody profiles and, in particular, the presence/absence and type of antibodies to cadherins determines the acantholytic signaling pathways [6,7] and possibly the clinical phenotype [8,9]. Despite advances in understanding the pathophysiology of these disorders, however, the mainstay of treatment is the use of corticosteroids and immune suppressants and, significantly, no mechanism-based treatments have been successfully translated to patient care.…”
Section: Introductionmentioning
confidence: 99%