Jean-Claude Bystryn 1938-2010. An obituary

Grando, Sergei A.; Holubar, Karl; Schwartz, Robert A.

doi:10.1111/j.1600-0625.2010.01214.x

Cited by 5 publications

(3 citation statements)

References 60 publications

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“…The antibody to the tumour necrosis factor (TNF) receptor superfamily member 5 (CD40) may contribute to induction of keratinocyte apoptosis (a.k.a. apoptolysis) in PV (19). The same may hold true for antibody against the nicotinamide adenine dinucleotide synthesizing enzyme NMNAT2, a.k.a.…”

Section: Resultsmentioning

confidence: 83%

New targets of pemphigus vulgaris antibodies identified by protein array technology

Kalantari-Dehaghi

Molina

Farhadieh

et al. 2011

Experimental Dermatology

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We performed partial evaluation of pemphigus vulgaris (PV) autoantibody profile using the protein array technology. The sera from seven patients with acute PV and five healthy donors were probed for the presence of autoantibodies characteristic of the organ-non-specific autoimmune disorders rheumatoid arthritis, lupus erythematosus, scleroderma, diabetes and some other autoimmune disorders, but not to desmosomal proteins. The array targeted 785 human genes amplified using Mammalian Gene Clone Collection with gene-specific primers containing 20-bp nucleotide extension complementary to ends of linear pXT7 vector. The array identified PV antibodies significantly (P < 0.05) differentially reactive with 16 antigens, most of which were cell-surface proteins, such as CD2, CD31, CD33, CD36, CD37, CD40, CD54, CD66c and CD84 molecules, nicotinamide ⁄ nicotinic acid mononucleotide adenylyltransferase, immunoglobulin heavy chain constant region gamma 2 and others. Reactivity with Fc-IgG helps explain an ability of the chimeric desmoglein constructs to absorb out all disease-causing PV antibodies. Anti-M 1 muscarinic receptor antibody was also identified, consistent with the facts that while blockade of this receptor causes keratinocyte detachment, its activation is therapeutic in PV. Further proteomics analysis of PV antibodies should help elucidate the immunopathogenic mechanisms underlying keratinocyte detachment and blistering.

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Section: Resultsmentioning

confidence: 83%

New targets of pemphigus vulgaris antibodies identified by protein array technology

Kalantari-Dehaghi

Molina

Farhadieh

et al. 2011

Experimental Dermatology

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“…Cell death is common in many skin diseases, such as sunburn, contact dermatitis, lupus erythematosus, lichen planus and many others (23)(24)(25) or after use of drugs (26). TEN, however, is unique in terms of the aggressiveness and extent of destruction of keratinocytes and also in mostly being caused by the adverse effects of medication.…”

Section: Discussionmentioning

confidence: 99%

Death ligand TRAIL, secreted by CD1a+ and CD14+ cells in blister fluids, is involved in killing keratinocytes in toxic epidermal necrolysis

Araujo

Dessirier

Laprée

et al. 2011

Experimental Dermatology

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Toxic epidermal necrolysis (TEN) is characterized by an acute detachment and destruction of keratinocytes, affecting large areas of the skin. It is often related to adverse drug reactions. Previous studies have shown that effector CD8+ T cells, which accumulate in the blister fluid, are functionally cytotoxic and act through a classical perforin/granzyme B pathway. It has recently been shown that these cytotoxic T cells also secrete granulysin peptide, which is lethal to keratinocytes. These cytotoxic T cells exert their killer activity against autologous keratinocytes in the presence of the drug. However, they are unlikely to be the only effectors of TEN. We therefore searched for soluble death factors in the blister fluids that might kill keratinocytes. We found that the amounts of interferon-γ, TRAIL and TNF-α proteins were significantly greater in TEN blister fluids than in all controls (normal sera, TEN sera, burns and Eosinophilic pustular folliculitis blister fluids) and TNF-like weak inducer of apoptosis (TWEAK) amounts are also greater in all controls except burns. We showed that these proteins acted in synergy to induce the death of keratinocytes in vitro. We also found that TRAIL and TWEAK were secreted by CD1a+ and CD14+ cells present in the blister fluids. Thus, in addition to MHC class I-restricted cytotoxic T lymphocytes (CTLs), which lyse keratinocytes, ligands secreted by non-lymphoid cells capable of inducing keratinocyte death in an MHC class I-independent manner, also seem to be present in the blister fluids of patients with TEN.

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“…Indeed, AMAs produced by PV patients disrupt the electron transfer chain, resulting in a loss of electrochemical gradient across the inner membrane, increase ROS production and reduce the ability of keratinocytes to respond to stress. Such abnormalities can trigger the cell death signalling cascade, wherein the executioner caspases cleave selected cell adhesion molecules, such as desmosomal cadherins, leading to both cell detachment (acantholysis) and death (apoptosis)the unique form of keratinocyte demise in PV tentatively termed apoptolysis (9).…”

mentioning

confidence: 99%

Jean-Claude Bystryn 1938-2010. An obituary

Cited by 5 publications

References 60 publications

New targets of pemphigus vulgaris antibodies identified by protein array technology

New targets of pemphigus vulgaris antibodies identified by protein array technology

Death ligand TRAIL, secreted by CD1a+ and CD14+ cells in blister fluids, is involved in killing keratinocytes in toxic epidermal necrolysis

The mitochondrion is a common target of disease pathophysiology in pemphigus and pemphigoid

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