Development Of Pemphigus Vulgaris Research Articles

Pemphigus vulgaris after COVID-19 infection and vaccination

Pemphigus vulgaris after COVID-19 infection and vaccination

P38 MAPK Signaling in Pemphigus: Implications for Skin Autoimmunity

p38 mitogen activated protein kinase (p38 MAPK) signaling plays a major role in the modulation of immune-mediated inflammatory responses and therefore has been linked with several autoimmune diseases. The extent of the involvement of p38 MAPK in the pathogenesis of autoimmune blistering diseases has started to emerge, but whether it pays a critical role is a matter of debate. The activity of p38 MAPK has been studied in great detail during the loss of keratinocyte cell-cell adhesions and the development of pemphigus vulgaris (PV) and pemphigus foliaceus (PF). These diseases are characterised by autoantibodies targeting desmogleins (Dsg). Whether autoantibody-antigen interactions can trigger signaling pathways (such as p38 MAPK) that are tightly linked to the secretion of inflammatory mediators which may perpetuate inflammation and tissue damage in pemphigus remains unclear. Yet, the ability of p38 MAPK inhibitors to block activation of the proapoptotic proteinase caspase-3 suggests that the induction of apoptosis may be a consequence of p38 MAPK activation during acantholysis in PV. This review discusses the current evidence for the role of p38 MAPK in the pathogenesis of pemphigus. We will also present data relating to the targeting of these cascades as a means of therapeutic intervention.

Acetylcholine receptor antibodies in patients with pemphigus vulgaris: Correlation with disease extent at the time of diagnosis and during follow-up

Several studies have tried to determine the relationship between autoantibodies against the acetylcholine receptor and the development of pemphigus vulgaris. In this study, we observed that antibody levels against the acetylcholine receptor are mildly elevated in pemphigus vulgaris (PV), and significantly correlate with disease severity on the initial diagnosis and during follow up. However, it is not clear if these antibodies are just an epiphenomenon or a potential trigger of the known pathogenic process in PV.

Roles of apoptosis in the development of pemphigus vulgaris

Pemphigus vulgaris was previously regarded as an pathogenic antibody-mediated autoimmune mucocutaneous disease. However, with the increase in knowledge about the pathogenesis of this entity, the roles of apoptosis in the development of pemphigus vulgaris have become more and more clear. For example, the apoptosis of keratinocytes can be induced by direct action of antibodies, and anoikis can be triggered by loss of cellular linkage following acantholysis. The hypothesis of apoptolysis further clarifies the correlation between apoptosis and acantholysis, and confirms that the apoptosis in pemphigus vulgaris is a unique paradigm of cell damage and detachment which should be distinguished from other classic known forms of cell death. These findings will facilitate the search of new targets for treatment of pemphigus vulgaris. Key words: Pemphigus, vulgaris; Apoptosis; Antibodies; Acantholysis

Development of pemphigus vulgaris in a patient with psoriasis treated with cyclosporine

Development of pemphigus vulgaris in a patient with psoriasis treated with cyclosporine

Development of pemphigus vulgaris in a patient with psoriasis treated with etanercept

Development of pemphigus vulgaris in a patient with psoriasis treated with etanercept

Frontiers in Nephrology

Natural killer (NK) cells are recognized for providing an important early innate immune response to viral and bacterial pathogens and for the surveillance of stressed and transformed autologous cells. However, with the exception of a pronounced role in allogeneic hematopoietic stem cell rejection, it has been challenging to ascribe the precise roles for NK cells in reactivity to tissue and solid-organ transplants. In general, NK cells initiate a rapid, proinflammatory environment that is conducive to many forms of effective immune host defense. This reactivity is often considered deleterious to allograft survival because NK cells are implicated in promoting both acute and chronic graft injury. However, more recent findings indicate that NK cells can also play a surprisingly profound role in allograft tolerance induction. This duality of function requires a reconsideration of the nature and consequence of NK cell reactivity during the allograft response. This review focuses on the differing "faces" of NK cells, especially the unexpected role of NK cells in allograft tolerance induction.

Development of pemphigus vulgaris in a patient with vitiligo and Hashimoto’s thyroiditis

Pemphigus vulgaris is an autoimmune blistering disease. An association of pemphigus vulgaris with vitiligo or Hashimoto's thyroiditis has not been reported before. We reported a 38 yr-old female patient with Hashimoto's thyroiditis and vitiligo who eventually developed pemphigus vulgaris on vitiliginous lesions. A genetic predisposition or a local event on vitiliginous skin may be responsible for the development of pemphigus in this patient.

Pemphigus vulgaris in siblings: HLA-DR4 and HLA-DQw3 and susceptibility to pemphigus

The association of pemphigus vulgaris with the HLA serotypes, DR4 and DRw6, and with the DQ-beta chain alleles, DQw1 and DQw3, suggests that there is a genetic predisposition to this disease. However, familial cases of pemphigus vulgaris are exceedingly rare. We studied two siblings with pemphigus vulgaris and three unaffected family members to determine whether an HLA allele was associated with the development of pemphigus vulgaris in this family. We utilized restriction fragment length polymorphism methods using the HLA-DR beta 1, HLA-DQ alpha, and HLA-DW beta 1 genes as cDNA probes. We found that the affected siblings share the haplotype HLA-DR4 and the DQw.3.2 allele. Our findings of gene sharing among siblings with pemphigus vulgaris lend support to previous studies of unrelated Caucasian patients, which implicated DQw3 allele polymorphisms in conferring susceptibility to pemphigus.