IgG, IgA and IgE autoantibodies against the ectodomain of desmoglein 3 in active pemphigus vulgaris

Spaeth, S.; Riechers, R.; Borradori, Luca; Zillikens, Detlef; Büdinger, Lioba; Hertl, Michael

doi:10.1046/j.1365-2133.2001.04228.x

Cited by 71 publications

(57 citation statements)

References 29 publications

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“…1D, E, F). In both PV and PF, patients with active disease demonstrate DSG-reactive IgG4 and IgG1, while patients in remission and some healthy relatives of pemphigus patients can demonstrate only anti-DSG IgG1 [27,28,37,72,73]. Probably IgG2 and IgG3 anti-DSG abs have not been associated with pemphigus [7,74].…”

Section: Discussionmentioning

confidence: 99%

“…However, recent studies have revealed that autoreactive T-cells show the features of Th1, as well as Th2, in patients with PV [21][22][23], PF [24] and BP [25,26]. Thus, probably both autoreactive Th1-and Th2-cells may be involved in the regulation of the production of pathogenic abs by B-cells in pemphigus/BP and in these patients autoimmunity against DSG-/DEJ-components may be Th1-regulated for IgG1 and Th2-regulated for IgG4 [27,28]. It is suggested that DSG3-and BP180-reactive Tcells, respectively in PV and BP, presumably foster the production of abs of the Th2-dependent IgG4 subtype, that are preferentially seen in active stages of these disorders [6].…”

Section: A B C Dmentioning

confidence: 99%

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Clinical immunology Immunoglobulin G4 is prevailing over immunoglobulin G1 in autoimmunity of pemphigus and bullous pemphigoid: analysis of tissue-bound antibodies in active diseases

Gornowicz‐Porowska¹,

Pietkiewicz²,

Bowszyc‐Dmochowska³

et al. 2013

cejoi

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Section: Discussionmentioning

confidence: 99%

Section: A B C Dmentioning

confidence: 99%

Clinical immunology Immunoglobulin G4 is prevailing over immunoglobulin G1 in autoimmunity of pemphigus and bullous pemphigoid: analysis of tissue-bound antibodies in active diseases

Gornowicz‐Porowska¹,

Pietkiewicz²,

Bowszyc‐Dmochowska³

et al. 2013

cejoi

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“…By magnetic cell sorting (MACS) cytokine secretion assay, Dsg3-reactive Th2 cells were detected at similar frequencies in acute onset, chronic active, and remittent PV, while the number of autoreactive Th1 cells exceeded that of Th2 cells in chronic active PV (18). Autoreactive Th1 and Th2 cells may be involved in the regulation of the production of pathogenic autoantibodies by B cells in PV since sera of patients with PV contain Th1-regulated IgG1 and Th2-regulated IgG4 autoantibodies directed against Dsg3 (Figure 3) (19,20).…”

Section: Autoreactive T Lymphocytes In Pemphigusmentioning

confidence: 99%

T cell control in autoimmune bullous skin disorders

Hertl¹

2006

Journal of Clinical Investigation

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198

129

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Autoimmune bullous disorders are a group of severe skin diseases characterized clinically by blisters and erosions of skin and/or mucous membranes. A hallmark of these disorders is the presence of IgG and occasionally IgA autoantibodies that target distinct adhesion structures of the epidermis, dermoepidermal basement membrane, and anchoring fibrils of the dermis. This Review focuses on the potential role of autoreactive T cells in the pathogenesis of these disorders. Pemphigus vulgaris (PV) and bullous pemphigoid (BP) are the best-characterized bullous disorders with regard to pathogenesis and T cell involvement. Activation of autoreactive T cells in PV and BP is restricted by distinct HLA class II alleles that are prevalent in individuals with these disorders. Autoreactive T cells are not only present in patients but can also be detected in healthy individuals. Recently, a subset of autoreactive T cells with remarkable regulatory function was identified in healthy individuals and to a much lesser extent in patients with PV, suggesting that the occurrence of autoimmune bullous disorders may be linked to a dysfunction of Tregs.Autoimmune bullous skin disorders are characterized by the presence of autoantibodies that target distinct adhesion molecules of the epidermis and dermoepidermal basement membrane zone, leading to a loss of adhesive function of the target antigen(s) and, clinically, to the appearance of blisters and erosions (1, 2) (Figures 1 and 2). Desmogleins are transmembranous components of desmosomes, adhesion units specialized in conferring epidermal keratinocyte cohesion and linked to intercellular molecules of the desmosomal plaque, which in turn interact with components of the cytoskeleton (Figure 1). In pemphigus, IgG autoantibodies against desmoglein 3 (Dsg3) and Dsg1 lead to loss of desmosomal adhesion of epidermal keratinocytes and intraepidermal blister formation (Figure 2). In the pemphigoids, IgG autoantibodies against components of the dermoepidermal basement membrane such as bullous pemphigoid (BP) antigen 180 (BP180; also referred to as BP antigen 2 and type XVII collagen), BP antigen 230 (BP230; also referred to as BP antigen 1), and laminin 5 interfere with the adhesion of basal epidermal keratinocytes to the dermoepidermal basement membrane zone (Figure 1). BP180 and BP230 are transmembranous and intracellular components, respectively, of hemidesmosomes of basal epidermal keratinocytes, while laminin 5 is a ligand of BP180 located in the lamina lucida of the basement membrane zone (Figure 1). The autoantigen of epidermolysis bullosa, type VII collagen, is the major component of anchoring fibrils that connect the dermoepidermal basement membrane with interstitial collagen bundles of the dermis (Figure 1). The autoantigen of dermatitis herpetiformis, epidermal transglutaminase, is targeted by autoantibodies of the IgA class in the papillary dermis (Figure 2).Based on the specificity of the targeted antigens, several clinically and immune serologically distinct bullous disorders have be...

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“…[131] In the same study, IgE-anti-desmoglein 3 was detected more frequently in the sera of patients with acute onset compared to chronic active pemphigus vulgaris. [131,132] In summary, IgE reactivity seems to be more relevant in the endemic form of pemphigus foliaceus than in pemphigus vulgaris. …”

Section: Other Pemphigoid Diseasesmentioning

confidence: 99%

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Beek

Schulze

Zillikens

et al. 2015

Expert Review of Clinical Immunology

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Autoimmune bullous diseases (AIBDs) are characterized by autoantibodies against structural proteins of the dermal-epidermal junction (in pemphigoid diseases) and the epidermal/ epithelial desmosomes (in pemphigus diseases). By far, the most common AIBD is bullous pemphigoid, which is immunopathologically characterized by autoantibodies against BP180 (type XVII collagen) and BP230. IgG and, to a lesser extent, IgA autoantibodies are the major autoantibody isotypes in these disorders. IgE autoantibodies are increasingly reported in particular in bullous pemphigoid. The development of specific and sensitive anti-BP180 IgE ELISA systems, the report of two experimental murine models employing IgE autoantibodies against BP180, and the successful treatment of bullous pemphigoid with the anti-IgE antibody omalizumab have raised interest in the role of IgE autoantibodies and the modulation of their production in AIBDs. Here, the relevance of IgE autoantibodies in the diagnosis, pathophysiology, and treatment decisions of AIBDs, with a focus on bullous pemphigoid, is reviewed. ARTICLE HISTORY

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IgG, IgA and IgE autoantibodies against the ectodomain of desmoglein 3 in active pemphigus vulgaris

Cited by 71 publications

References 29 publications

Clinical immunology Immunoglobulin G4 is prevailing over immunoglobulin G1 in autoimmunity of pemphigus and bullous pemphigoid: analysis of tissue-bound antibodies in active diseases

Clinical immunology Immunoglobulin G4 is prevailing over immunoglobulin G1 in autoimmunity of pemphigus and bullous pemphigoid: analysis of tissue-bound antibodies in active diseases

T cell control in autoimmune bullous skin disorders

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

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