The distribution of pemphigus vulgaris-IgG subclasses and their reactivity with desmoglein 3 and 1 in pemphigus patients and their first-degree relatives

Kricheli, D; David, Michael; Frušić-Zlotkin, Marina; Goldsmith, D.; Rabinov, M; Sulkes, Jacqueline; Milner, Yoram

doi:10.1046/j.1365-2133.2000.03659.x

Cited by 109 publications

(107 citation statements)

References 48 publications

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“…The main histopathological characteristic of PV is acantholysis of epidermis provoked by the disruption of keratinocyte intercellular interactions. This disruption seems to be a consequence of signaling pathways triggered by the binding of PV-IgG antibodies to keratinocytes, as has been shown by different in vivo and in vitro studies [22][23][24]. Therefore, PVIgG antibodies were able to produce in cultured HaCaT keratinocytes an effect similar to the features observed in animal models of PV and human patients affected by this disease.…”

Section: Pv-igg Provokes Disruption Of Cell-cell Contacts In Hacatsupporting

confidence: 51%

Pemphigus vulgaris autoantibodies induce apoptosis in HaCaT keratinocytes

PELACHO¹

2004

FEBS Letters

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Pemphigus vulgaris (PV) is an autoimmune disease characterized by binding of IgG autoantibodies to epidermal keratinocyte desmosomes. IgG autoantibodies obtained from a patient with mucocutaneous PV reacted with plakoglobin (Plkg) in addition to desmoglein-3 (Dsg3) and Dsg1. Immunofluorescence analysis confirmed that IgG autoantibodies, unlike antibodies from a healthy volunteer, caused disruption of cell-cell contacts in HaCaT keratinocytes. Moreover, apoptosis was enhanced in cells treated with autoantibodies compared to those treated with normal antibodies. The apoptotic process induced by IgG autoantibodies was characterized by caspase-3 activation, Bcl-2 depletion and Bax expression. The present report demonstrates that PV IgG autoantibodies promote apoptosis in HaCaT keratinocytes.

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Section: Pv-igg Provokes Disruption Of Cell-cell Contacts In Hacatsupporting

confidence: 51%

Pemphigus vulgaris autoantibodies induce apoptosis in HaCaT keratinocytes

PELACHO¹

2004

FEBS Letters

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“…Indeed, the pathogenic role of autoreactive IgG4 is suspected in several autoimmune diseases, particularly dermatological bullous diseases. IgG4 towards the major autoantigens of such diseases were reported to be associated to clinical features: to disease progression and severity in Pemphigus vulgaris [53,54], to progression from a preclinical to a clinical form in P. foliaceus [55], and to a long disease duration in bullous pemphigoid [56]. Finally, IgG1 in mice (the human IgG4 counterpart) may trigger immune effector functions via FcgRIII [42], supporting our hypothesis that a particular interaction between AhFibA subclasse(s) and particular type(s) of IgG receptors may be critical in the self-maintenance of inflammation.…”

Section: Discussionmentioning

confidence: 99%

IgG subclass distribution of the rheumatoid arthritis-specific autoantibodies to citrullinated fibrin

Chapuy‐Regaud

Nogueira

Clavel

et al. 2005

Clinical and Experimental Immunology

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SummaryIn the rheumatoid synovium, deiminated ('citrullinated') forms of fibrin are the major targets of IgG autoantibodies to citrullinated proteins (ACPA), the most specific serological markers of rheumatoid arthritis (RA). To further the characterization of ACPA, we determined their subclass distribution. From a previously validated highly sensitive and specific enzyme-linked immunosorbent assay (ELISA) onto in vitro deiminated human fibrinogen ----antihuman fibrin(ogen) autoantibodies (AhFibA)-ELISA ----we derived and calibrated four ELISAs, using monoclonal antibodies to each of the four IgG subclasses, to determine the proportions of AhFibA subclasses in the sera. A series of 186 serum samples from RA patients was analysed. All AhFibA-positive sera contained IgG1-AhFibA, which reached the highest titres and accounted for more than 80% of AhFibA in three-quarters of the sera. One or two other subclasses were associated with IgG1 in 39% of the sera, IgG4-AhFibA being observed much more frequently and at higher titres than IgG3-or IgG2-AhFibA. IgG1 alone or IgG(1 + 4)-AhFibA were the AhFibA subclass profiles found in more than 80% of patients. AhFibA are mainly IgG1 and, to a lesser extent, IgG4. Such IgG subclass profiles may influence the effector phases of the immunological conflict between ACPA and deiminated fibrin that takes place specifically in the rheumatoid synovium and therefore may play a critical role in the self-maintenance of rheumatoid inflammation.

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“…Previously, it was demonstrated that the main isotypes of tissue-bound and circulating abs are IgG4 and IgG1 in both pemphigus and BP [8,[35][36][37], but the role of Th1/Th2-cells as target for specific modulation of T-cell-dependent production of pathogenic auto-abs in these disorders still remains a matter of debate. It is reported that intraepidermal blister formation in pemphigus group is caused by binding of IgG to keratinocyte cells without engaging innate immune effectors, and IgG4 abs seem to mainly mediate acantholysis [16].…”

Section: A B C Dmentioning

confidence: 99%