Prevalence of Non–Organ-Specific Autoantibodies in Patients with Pemphigus Vulgaris

Blondin, David; Zhang, Zuhui; Shideler, Karalee K.; Hou, Hanxue; Fritzler, Marvin J.; Mydlarski, P. Régine

doi:10.2310/7750.2008.08001

Cited by 10 publications

(11 citation statements)

References 35 publications

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“…A large spectrum of organ-non-specific antigens that can be targeted by pemphigus autoimmunity (Table I) has been recently reviewed [39,65,66]. Although contribution of organ-non-specific antigens to keratinocyte detachment and death in pemphigus remains to be elucidated, it is plausible to speculate that some of them, e.g.…”

Section: Pemphigus Autoantigensmentioning

confidence: 99%

Pemphigus autoimmunity: Hypotheses and realities

2011

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The goal of contemporary research in pemphigus vulgaris and pemphigus foliaceus is to achieve and maintain clinical remission without corticosteroids. Recent advances of knowledge on pemphigus autoimmunity scrutinize old dogmas, resolve controversies, and open novel perspectives for treatment. Elucidation of intimate mechanisms of keratinocyte detachment and death in pemphigus has challenged the monopathogenic explanation of disease immunopathology. Over 50 organ-specific and non-organ-specific antigens can be targeted by pemphigus autoimmunity, including desmosomal cadherins and other adhesion molecules, PERP cholinergic and other cell membrane (CM) receptors, and mitochondrial proteins. The initial insult is sustained by the autoantibodies to the cell membrane receptor antigens triggering the intracellular signaling by Src, epidermal growth factor receptor kinase, protein kinases A and C, phospholipase C, mTOR, p38 MAPK, JNK, other tyrosine kinases, and calmodulin that cause basal cell shrinkage and ripping desmosomes off the CM. Autoantibodies synergize with effectors of apoptotic and oncotic pathways, serine proteases, and inflammatory cytokines to overcome the natural resistance and activate the cell death program in keratinocytes. The process of keratinocyte shrinkage/detachment and death via apoptosis/oncosis has been termed apoptolysis to emphasize that it is triggered by the same signal effectors and mediated by the same cell death enzymes. The natural course of pemphigus has improved due to a substantial progress in developing of the steroid-sparing therapies combining the immunosuppressive and direct anti-acantholytic effects. Further elucidation of the molecular mechanisms mediating immune dysregulation and apoptolysis in pemphigus should improve our understanding of disease pathogenesis and facilitate development of steroid-free treatment of patients.

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Section: Pemphigus Autoantigensmentioning

confidence: 99%

Pemphigus autoimmunity: Hypotheses and realities

2011

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“…Clinical observations demonstrated that co-manifestation of autoimmune disease within a single patient occurs more frequently than combined prevalence of underlying diseases predicts (7). Furthermore, patients with autoimmune disease are prone to develop additional autoantibody reactivities, for example an increased frequency of (i) anti-thyroid antibodies were found in rheumatoid arthritis (8); (ii) antinuclear antibodies (ANA) in pemphigus (9); or (iii) anti-CCP antibodies in rheumatoid arthritis (10). In contrast, it is not known whether different autoantibodies co-occur in individuals who are clinically healthy.…”

Section: Introductionmentioning

confidence: 99%

“…Several studies have suggested that MSCs have pleiotropic immunomodulatory effects, including the inhibition of T cell proliferation (4-6), suppression of natural killer (NK) cell proliferation (7), modulation of cytokine production (8), and inhibition of dendritic cell (DC) maturation (9,10). Although many soluble factors such as transforming growth factor-beta (TGF-b) (11,12) and IL-10 (13) have been reported to be involved in the immunomodulatory effects of MSCs, the exact mechanism underlying immunosuppression by MSCs remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Co‐occurrence of autoantibodies in healthy blood donors

Prüßmann

Recke

et al. 2014

Experimental Dermatology

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Autoimmune diseases are rare, but their incidence has increased over the past decades. Interestingly, the co-occurrence of autoimmune diseases is well documented; however, data on the presence of more than one specific autoantibody in healthy individuals are not available. Here, we investigated the prevalence of several autoantibodies in a cohort of over 6000 healthy persons. While individual autoantibodies were rarely detected (i.e. ranging from 0.3% for ANCA to 4.6% for anti-TPO), the cumulative prevalence of the tested autoantibodies was as high as 10%. Furthermore, our results demonstrate co-occurrence of ANA with specific autoantibodies that target TPO, CCP and Dsg1/3, while ANCA and autoantibodies to PCA and BP180/BP230 were not more frequent in ANA-positive compared to ANA-negative samples. This indicates that shared and independent mechanisms influence loss of tolerance to distinct sets of self-antigens.

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“…Our results corroborate with findings obtained in other series, showing that ASMA, RF, AMA, GPCA and LKM1 positivity is not frequent in pemphigus. [5] Concerning ANA, their prevalence was low in our pemphigus cohort and, in the literature, there are conflicting results concerning its presence in pemphigus patients. [1,2] This may be explained by a variation in the genetic background of the cohorts, It is worth noticing that corticosteroids and/or immunosuppressive treatment in 57.5% of the patients of our study should be considered as important as it may have interfered with the positivity of circulating autoantibodies.…”

Section: Prevalence Of Autoantibodies In Patients With Pemphigusmentioning

confidence: 63%

“…Such data are mainly based on isolated case reports or on serologic surveys using a limited number of autoantibodies. [1][2][3][4][5] Data related to the prevalence of nonorgan-specific autoantibodies in pemphigus are often lacking.…”

Section: Prevalence Of Autoantibodies In Patients With Pemphigusmentioning

confidence: 99%