A Canine Pemphigus Foliaceus Case Showing Parallel Relationship of Disease Activity and Titer of Serum Anti-keratinocyte Cell Surface Antibodies

Section: Discussioncontrasting

confidence: 99%

Evaluation of C‐reactive protein as an inflammatory marker of pemphigus foliaceus and superficial pyoderma in dogs

Severo

Santana

Aoki

et al. 2017

“…In six dogs, immunosuppression led to a reduction in clinical scores with serum IgG, IgG1 and IgG4 autoantibody titres decreasing in four, one and four patients, respectively 59 . Similarly, serum titres of IgG autoantibodies correlated with the severity of clinical signs of canine PF in two recent reports from the same group 22,60 …”

Section: Pemphigus Foliaceusmentioning

confidence: 61%

A review of autoimmune skin diseases in domestic animals: I – Superficial pemphigus

Olivry

2006

158

In humans, the pemphigus denomination encompasses a group of autoimmune blistering skin diseases with intraepidermal separation resulting from cell-cell detachment by acantholysis. Entities are classified based on the level of blistering in the epidermis, and both superficial (pemphigus foliaceus, IgA pemphigus) and deep (pemphigus vulgaris, pemphigus vegetans and paraneoplastic pemphigus) variants are recognized. In domestic animals, subsets of pemphigus have been recognized since the mid-1970s, and the disease classification resembles that used for human patients. This article reviews up-to-date knowledge on the epidemiology, clinical signs, histopathology, immunopathology and treatment outcome of superficial pemphigus in domestic animals. Detailed information on canine, feline, equine and caprine pemphigus foliaceus, canine and feline pemphigus erythematosus and canine panepidermal pustular pemphigus is provided.

“…In dogs with PF, appropriate substrates for indirect IF have been reported to be bovine oesophagus 13 and dog keratinocyte cultures 14,15 . Using one of these substrates, Nishifuji and colleagues established that IgG autoantibody titres correlated with clinical disease in one dog with PF 16 …”

Section: Introductionmentioning

confidence: 99%

Investigations on the nature and pathogenicity of circulating antikeratinocyte antibodies in dogs with pemphigus foliaceus

Olivry

Dunston

Walker

et al. 2009

In humans with pemphigus foliaceus (PF), pathogenic autoantibodies are principally of IgG4 subclass and they cause superficial vesiculation when injected into neonatal mice. The objectives of this study were to determine the isotypes of circulating antikeratinocyte antibodies in dogs with PF, to assess whether serum antikeratinocyte antibody titres decreased during successful treatment, and to study whether such antibodies were pathogenic in passive transfers. Using indirect immunofluorescence with neonatal mouse skin substrates, circulating antikeratinocyte IgG antibodies were detected in 36 of 44 dogs with PF (82%). Serum autoantibodies belonged predominantly to IgG4 (three of 44; 80%) and IgG1 (30 of 44; 68%) subclasses. Antikeratinocyte IgG antibodies were detected in 16 of 20 normal dogs (80%), and these antibodies were IgG1 (16 of 20, 80%) but rarely IgG4 (two of 20; 10%) isotypes. In four dogs, IgG4 antikeratinocyte antibody titres decreased concomitantly to lesions nearing or reaching complete remission. In contrast, IgG or IgG1 titres remained stable or increased when lesions abated. Antikeratinocyte antibodies targeted mainly intercellular autoantigen(s) in the stratum granulosum, while in fewer dogs, such antibodies bound to cytoplasmic basal antigen(s). Intradermal injections of PF or pemphigus vulgaris (PV) IgG into neonatal mice caused subgranular or suprabasal acantholytic vesiculation without granulocyte infiltration, respectively. Similar transfers of normal dog IgG did not cause vesiculation. These observations suggest that antikeratinocyte IgG4 antibodies could be relevant to disease pathogenesis. Importantly, canine PF or PV IgG appear to be pathogenic when transferred passively into mice, causing vesiculation at epidermal levels similar to those of the natural disease.