Serum Levels of Inhibitors of Apoptotic Proteins (IAPs) Change with IVIg Therapy in Pemphigus

Toosi, Siavash; Habib, Nancy; Torres, Genevieve; Reynolds, Sandra R.; Bystryn, Jean‐Claude

doi:10.1038/jid.2011.184

Cited by 5 publications

(2 citation statements)

References 14 publications

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“…Interestingly, NHuK and HSOC treated with PV-IgG and/or Fas-L and TNF presented increased cell death and acantholysis [ 104 ]. Finally, serum levels of the apoptosis inhibitors livin and X-linked inhibitor of apoptotic proteins (XIAP) increased in all seven investigated pemphigus patients (5 PV and 2 PF) after IVIg treatment [ 118 ]. Interestingly, pathogenic anti-Dsg3 antibodies activate apoptosis in a FasL-independent way in cultured keratinocytes, increasing combined Annexin V and propidium iodide (PI) positivity at 4 h, with a peak at 12 h post-treatment.…”

Section: Resultsmentioning

confidence: 99%

“…Acantholytic cells of 17 PV biopsies presented CASP3 gene and protein expression [ 105 ], and both lesional and perilesional epidermis and dermis from PV patients presented an increased number of cells with activated CASP-3 [ 80 , 109 ]. Higher CASP-1 and/ or CASP-3 expression was detected in NhuK and HSOC treated/ injected with PV-IgG [ 19 , 24 , 118 , 119 ], although the opposite for CASP-3 was true in another study [ 68 ]. After treatment of NhuK with PV-IgG, activated CASP-3 increased concomitantly with cell death (evaluated by methylene blue) and acantholysis [ 89 ].…”

Section: Resultsmentioning

confidence: 99%

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Marked to Die-Cell Death Mechanisms for Keratinocyte Acantholysis in Pemphigus Diseases

Bumiller-Bini

Schneider

Pumpe

et al. 2022

Life

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Pemphigus is a group of blistering autoimmune diseases causing painful skin lesions, characterized by acantholysis and by the production of autoantibodies against, mainly, adhesion proteins. We reviewed the literature for molecules and/ or features involved in the 12 cell death pathways described by Nomenclature Committee on Cell Death, taking place in pemphigus patients, cell lines, or human skin organ cultures treated with sera or IgG from pemphigus patients or in pemphigus mouse models, and found 61 studies mentioning 97 molecules involved in cell death pathways. Among the molecules, most investigated were pleiotropic molecules such as TNF and CASP3, followed by FASL and CASP8, and then by FAS, BAX, BCL2, and TP53, all involved in more than one pathway but interpreted to function only within apoptosis. Most of these previous investigations focused only on apoptosis, but four recent studies, using TUNEL assays and/or electron microscopy, disqualified this pathway as a previous event of acantholysis. For PV, apoptolysis was suggested as a cell death mechanism based on pathogenic autoantibodies diversity, mitochondrial dysfunction, and p38 MAPK signaling. To answer those many questions that remain on cell death and pemphigus, we propose well-controlled, statistically relevant investigations on pemphigus and cell death pathways besides apoptosis, to overcome the challenges of understanding the etiopathology of pemphigus diseases.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Marked to Die-Cell Death Mechanisms for Keratinocyte Acantholysis in Pemphigus Diseases

Bumiller-Bini

Schneider

Pumpe

et al. 2022

Life

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Apoptosis and Signaling in Bullous Diseases: Pemphigus

Rubenstein

Pincelli

2015

Blistering Diseases

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Pemphigus

Eming

2015

Hautarzt

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The well-characterised basic pathogenesis of pemphigus results in targeted therapies. Currently, therapies aiming at rapid reduction of circulating autoantibodies and the depletion of autoreactive B-cells are in clinical use. More cellular and molecular target structures are being investigated in other autoantibody-driven autoimmune disorders and they provide promising candidates for innovative pathogenesis-related therapeutic strategies in pemphigus in the future.

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Serum Levels of Inhibitors of Apoptotic Proteins (IAPs) Change with IVIg Therapy in Pemphigus

Cited by 5 publications

References 14 publications

Marked to Die-Cell Death Mechanisms for Keratinocyte Acantholysis in Pemphigus Diseases

Marked to Die-Cell Death Mechanisms for Keratinocyte Acantholysis in Pemphigus Diseases

Apoptosis and Signaling in Bullous Diseases: Pemphigus

Pemphigus

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