Walnut antigens can trigger autoantibody development in patients with pemphigus vulgaris through a “hit-and-run” mechanism

Lin, Lan; Moran, Timothy P.; Peng, Bin; Yang, Jinsheng; Culton, Donna A.; Che, Huilian; Jiang, Songsong; Liu, Zhi; Geng, Songmei; Zhang, Yuzhu; Díaz, Luis A.; Qian, Yuping

doi:10.1016/j.jaci.2019.04.020

Cited by 21 publications

(14 citation statements)

References 59 publications

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“…Certain allergens may lead to autoimmune responses. Walnut antigens or allergens have been reported to initiate the development of autoantibodies in pemphigus vulgaris via a “hit-and-run” pattern, meaning that pathogenic antigens causing the onset of autoimmune conditions disappear once they have triggered the disease [ 25 ]. Kridin et al.…”

Section: Pemphigusmentioning

confidence: 99%

The pathogenesis of bullous skin diseases

Yang

Zhao

et al. 2019

Journal of Translational Autoimmunity

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Bullous skin diseases are a group of dermatoses characterized by blisters and bullae in the skin and mucous membranes. The etiology and pathogenesis of bullous skin diseases are not completely clear. The most common are pemphigus and bullous pemphigoid (BP). Autoantibodies play critical roles in their pathogenesis. Abnormalities in the adhesion between keratinocytes in patients with pemphigus leads to acantholysis and formation of intra-epidermal blisters. Anti-desmoglein autoantibodies are present both in the circulation and skin lesions of patients with pemphigus. The deficient adhesion of keratinocytes to the basement membrane in BP patients gives rise to subepidermal blisters. Autoantibodies against the components of hemidesmosome can be detected in BP patients. Many novel therapeutics based on knowledge of the pathogenesis have emerged in recent years.

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Section: Pemphigusmentioning

confidence: 99%

The pathogenesis of bullous skin diseases

Yang

Zhao

et al. 2019

Journal of Translational Autoimmunity

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“…In contrast, germline-reverted mAbs were generally unable to bind Dsg3, indicating that disease-causing MBCs likely originate from non-autoreactive B cell precursors or naive cells of very low affinity. It remains unclear what initial trigger activates these precursors, although it is possible that molecular mimicry may drive initial responses against Dsg3 (Cho et al, 2016; Lin et al, 2019), which is also a mechanism proposed for the related endemic form of pemphigus, fogo selvagem (Qian et al, 2012). While previous publications have shown that some germline-reverted mAbs with V H 1-46 gene usage are able to bind to Dsg3 (Cho et al, 2014), none of our V H 1-46 mAbs retained binding activity in germline form.…”

Section: Discussionmentioning

confidence: 99%

Single-Cell Analysis Suggests that Ongoing Affinity Maturation Drives the Emergence of Pemphigus Vulgaris Autoimmune Disease

et al. 2019

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SUMMARY Pemphigus vulgaris (PV) is an autoimmune disease characterized by blistering sores on skin and mucosal membranes, caused by autoantibodies primarily targeting the cellular adhesion protein, desmoglein-3 (Dsg3). To better understand how Dsg3-specific autoantibodies develop and cause disease in humans, we performed a cross-sectional study of PV patients before and after treatment to track relevant cellular responses underlying disease pathogenesis, and we provide an in-depth analysis of two patients by generating a panel of mAbs from single Dsg3-specific memory B cells (MBCs). Additionally, we analyzed a paired sample from one patient collected 15-months prior to disease diagnosis. We find that Dsg3-specific MBCs have an activated phenotype and show signs of ongoing affinity maturation and clonal selection. Monoclonal antibodies (mAbs) with pathogenic activity primarily target epitopes in the extracellular domains EC1 and EC2 of Dsg3, though they can also bind to the EC4 domain. Combining antibodies targeting different epitopes synergistically enhances in vitro pathogenicity.

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“…36 In pemphigus, Dsg-specific autoantibodies have been shown to cross-react with pathogen-directed antibodies 13,110,111 or in a recent report with walnut antigens. 112 Also, T-cell-driven ncISDs have been associated with molecular mimicry. An exanhematic form of psoriasis, so-called guttate psoriasis, is often triggered by streptococcal infections.…”

Section: ) Aberrant Expression Of Antigens or Neoantigen Formationmentioning

confidence: 99%

Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin

Guðjónsson

Kabashima

Eyerich

2020

Journal of Allergy and Clinical Immunology

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Walnut antigens can trigger autoantibody development in patients with pemphigus vulgaris through a “hit-and-run” mechanism

Cited by 21 publications

References 59 publications

The pathogenesis of bullous skin diseases

The pathogenesis of bullous skin diseases

Single-Cell Analysis Suggests that Ongoing Affinity Maturation Drives the Emergence of Pemphigus Vulgaris Autoimmune Disease

Mechanisms of skin autoimmunity: Cellular and soluble immune components of the skin

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