Anti-Desmoglein 1 and 3 Autoantibody Levels in Endemic Pemphigus Foliaceus and Pemphigus Vulgaris from Brazil

Oliveira, Liana Alves de; Marquart-Filho, Alfredo; Trevilato, Gerson; Timóteo, Rodolfo Pessato; Mukai, Maira Mitsue; Roselino, Ana Maria Ferreira; Petzl-Erler, María Luiza

doi:10.7754/clin.lab.2015.150628

Cited by 8 publications

(8 citation statements)

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“…These autoantigens are mainly two desmosomal cadherins: desmoglein (DSG) 1 and/or DSG3. Two main forms of pemphigus usually associate to autoAb profiles ( 9 – 12 ). In pemphigus foliaceus (PF), typically only anti-DSG1 autoAb, superficial blistering and erosions are observed.…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between Signaling Pathways in Pemphigus: A Role for Endoplasmic Reticulum Stress in p38 Mitogen-Activated Protein Kinase Activation?

et al. 2017

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Pemphigus consists of a group of chronic blistering skin diseases mediated by autoantibodies (autoAbs). The dogma that pemphigus is caused by keratinocyte dissociation (acantholysis) as a distinctive and direct consequence of the presence of autoAb targeting two main proteins of the desmosome—desmoglein (DSG) 1 and/or DSG3—has been put to the test. Several outside-in signaling events elicited by pemphigus autoAb in keratinocytes have been described, among which stands out p38 mitogen-activated protein kinase (p38 MAPK) engagement and its apoptotic effect on keratinocytes. The role of apoptosis in the disease is, however, debatable, to an extent that it may not be a determinant event for the occurrence of acantholysis. Also, it has been verified that compromised DSG trans-interaction does not lead to keratinocyte dissociation when p38 MAPK is inhibited. These examples of conflicting results have been followed by recent work revealing an important role for endoplasmic reticulum (ER) stress in pemphigus’ pathogenesis. ER stress is known to activate the p38 MAPK pathway, and vice versa. However, this relationship has not yet been studied in the context of activated signaling pathways in pemphigus. Therefore, by reviewing and hypothetically connecting the role(s) of ER stress and p38 MAPK pathway in pemphigus, we highlight the importance of elucidating the crosstalk between all activated signaling pathways, which may in turn contribute for a better understanding of the role of apoptosis in the disease and a better management of this life-threatening condition.

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Section: Introductionmentioning

confidence: 99%

Crosstalk between Signaling Pathways in Pemphigus: A Role for Endoplasmic Reticulum Stress in p38 Mitogen-Activated Protein Kinase Activation?

et al. 2017

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“…We measured sCR1 levels in the serum (collected without anticoagulant) by using a SEB123Hu ELISA kit (USCN Life Science Inc., Wuhan, China) according to the manufacturer's instructions. Anti-Dsg1 and anti-Dsg3 levels were previously measured using commercial ELISA kits (RG-M7593-D and RG-7680-EC-D, respectively) (MBL, Woburn, USA) (43).…”

Section: Methodsmentioning

confidence: 99%

Complement Receptor 1 (CR1, CD35) Polymorphisms and Soluble CR1: A Proposed Anti-inflammatory Role to Quench the Fire of “Fogo Selvagem” Pemphigus Foliaceus

et al. 2019

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Pemphigus foliaceus is an autoimmune disease that is sporadic around the world but endemic in Brazil, where it is known as fogo selvagem (FS). Characterized by autoantibodies against the desmosomal cadherin desmoglein 1, FS causes painful erosions, and crusts that may be widespread. The recognition of antigens, including exposed sugar moieties, activates the complement system. Complement receptor 1 (CR1, CD35), which is responsible for the Knops blood group on erythrocytes (York and McCoy antigens), is also expressed by antigen-presenting cells. This regulates the complement system by removing opsonized antigens, blocking the final steps of the complement cascade. Membrane-bound CR1 also fosters antigen presentation to B cells, whereas soluble CR1 has anti-inflammatory properties. CR1 gene polymorphisms have been associated with susceptibility to complex diseases. In order to investigate the association of CR1 polymorphisms with FS susceptibility, we developed a multiplex sequence-specific assay to haplotype eleven polymorphisms in up to 367 FS patients and 242 controls from an endemic area and 289 from a non-endemic area. We also measured soluble CR1 (sCR1) in the serum of 53 FS patients and 27 controls and mRNA levels in the peripheral blood mononuclear cells of 63 genotyped controls. The haplotypes CR1*3B2B (with the York antigen–encoded by p.1408Met) and CR1*3A2A (with p.1208Arg) were associated with protection against FS (OR = 0.57, P = 0.027, and OR = 0.46, P = 0.014, respectively). In contrast, the CR1*1 haplotype (with the McCoy antigen – encoded by p.1590Glu) was associated with FS susceptibility (OR = 4.97, P < 0.001). Heterozygote rs12034383*A/G individuals presented higher mRNA expression than homozygotes with the G allele (P = 0.04). The lowest sCR1 levels occurred in patients with active disease before treatment (P = 0.036). Patients in remission had higher levels of sCR1 than did healthy controls (P = 0.013). Among those under treatment, patients with localized lesions also presented higher sCR1 levels than those with generalized lesions (P = 0.0073). In conclusion, the Knops blood group seems to modulate susceptibility to the disease. Furthermore, corticosteroid treatment might increase sCR1 serum levels, and higher levels may play an anti-inflammatory role in patients with FS, limiting the distribution of lesions. Based on these results, we suggest CR1 as a potential new therapeutic target for the treatment of FS.

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“…Nevertheless, another BP patient with oral lesions did not present anti‐DSG3 antibodies. Additionally, anti‐DSG antibodies have been described in Brazilian healthy populations . Thus, anti‐DSG antibodies in Brazilian BP patients deserve special attention.…”

Section: Clinical and Laboratory Data Of Four Patients With Bullous Pmentioning

confidence: 99%

Anti‐desmogleins autoantibodies detected by ELISA and blotting in bullous pemphigoid: what do they mean?

et al. 2017

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In addition to antibiotics, whirlpool therapy can be used to treat erythrodermic flares of MF/SS because it reduces bacterial colonization and debrides excess scale. 5 It also decreases inflammation and promotes wound cleansing. 6 Moreover, a pilot study showed that whirlpool therapy followed by a quick rinse eradicated more than four times as many bacteria compared with whirlpool therapy alone. 7 In our protocol, the 0.25% acetic acid rinse further decreases the skin bacterial load and reduces skin pH, which inhibits S. aureus colonization.

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Anti-Desmoglein 1 and 3 Autoantibody Levels in Endemic Pemphigus Foliaceus and Pemphigus Vulgaris from Brazil

Abstract: Despite the importance of these antibodies for diagnosis and management purposes, their presence in a healthy individual and in patients under remission indicates that caution should be taken when using anti-DSG for diagnosis, especially in endemic areas.

Cited by 8 publications

References 0 publications

Crosstalk between Signaling Pathways in Pemphigus: A Role for Endoplasmic Reticulum Stress in p38 Mitogen-Activated Protein Kinase Activation?

Crosstalk between Signaling Pathways in Pemphigus: A Role for Endoplasmic Reticulum Stress in p38 Mitogen-Activated Protein Kinase Activation?

Complement Receptor 1 (CR1, CD35) Polymorphisms and Soluble CR1: A Proposed Anti-inflammatory Role to Quench the Fire of “Fogo Selvagem” Pemphigus Foliaceus

Anti‐desmogleins autoantibodies detected by ELISA and blotting in bullous pemphigoid: what do they mean?

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