Development of a disease registry for autoimmune bullous diseases: initial analysis of the pemphigus vulgaris subset.

Pemphigus vulgaris (PV) is a rare, potentially life threatening, autoimmune blistering skin disease. The International Pemphigus and Pemphigoid Foundation (IPPF) has recently developed a disease registry with the aim to enhance our understanding of autoimmune bullous diseases with the long-term goal of acquiring information to improve patient care. Patients were recruited to the IPPF disease registry through direct mail, e-mail, advertisements, and articles in the IPPF-quarterly, -website, -Facebook webpage, and IPPF Peer Health Coaches to complete a 38-question survey.

Cytokine pathways and interactions in alopecia areata.

Alopecia areata (AA) is an autoimmune disease resulting in the premature arrest of the follicular growth cycle clinically resulting in patchy, non-scarring hair loss. The presence of a dense follicular T cell infiltrate and variations in cytokines have led to the hypothesis that T cell activation and alterations in inflammatory mediators are crucial participants in the etiopathogenesis of the disease. Various studies suggest that the AA pathogenesis has a dominant TH1-mediated component, with potential involvement of the TH17 pathway.

Oxidative stress and autoimmune skin disease.

Antioxidants play the important role in our body of neutralizing free radicals and peroxides that are formed during normal physiologic events. While these reactive oxygen species are necessary for numerous biological processes, when created in excess they can have deleterious effects. The skin as an organ is constantly under attack by reactive oxygen species from both endogenous and exogenous sources.

HLA-E*0103X is associated with susceptibility to Pemphigus vulgaris.

Non-classical human leucocyte antigen-E (HLA-E) mediates natural killer and CD8+ T-cell activity, suggesting a role in the regulation of autoimmunity. HLA-E*0103X/*0103X has been associated with Behcet's disease and HLA-E *0101/*0103X with childhood onset diabetes. We investigated HLA-E allele status in 52 Caucasian and Ashkenazi Jewish Pemphigus vulgaris (PV) patients and 51 healthy controls by restriction fragment length polymorphism-polymerase chain reaction and amplification refractory mutation system.

Exploring the link between herpes viruses and pemphigus vulgaris: literature review and commentary.

Pemphigus vulgaris (PV) is an autoimmune skin condition characterized by the presence of circulating autoantibodies specific for a subset of cellular adhesion proteins within mucosal and/or non-mucosal epidermal surfaces. Although the presence of self-directed antibodies is well established, the exact etiology of PV is still uncertain. Environmental factors have been linked to a variety of autoimmune disorders.

Constructing immunoprofiles to deconstruct disease complexity in pemphigus.

The complex etiology of multifactorial diseases such as pemphigus vulgaris complicates mechanistic investigations and confounds current therapeutic approaches. Two major sources contribute to the overall complexity of disease. Biological complexity involves the disruption of multiple immune pathways that underlie autoimmune destruction in the skin.