A case of refractory chronic rhinosinusitis with anti-desmoglein 3 IgG4 autoantibody

Ota, Yasushi; Ishikawa, Fumio; Sato, Toshiya; Hiruta, Nobuyuki; Kikuchi, Makoto; Yokota, Hiromitsu; Ikemiyagi, Yoshihiro; Bujo, Hideaki; Fujiwara, Mutsunori; Suzuki, Michitaka

doi:10.1016/j.alit.2017.04.009

Cited by 5 publications

(1 citation statement)

References 9 publications

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“…anti-BP180(BPA2/collagen XVII) affect the adhesion of the stratified epithelia to the basement membrane [9] anti-periplakin IgE inhibit epithelial repair and lead to chronic airway epithelial injury [14] anti-phospholipid(APA) increase the fibrin deposition that forms the matrix of a nasal polyp [13] anti-phosphatidylethanolamine (anti-PE) associate with coagulation-induced pathology [13] anti-IL-5 maintain Th2 inflammation [12] anti-IL-17 exert its proallergic effect at the level of B cells, regulate Th2-skewed inflammation [12] anti-dsDNA trigger recurrent inflammation. [6] anti-desmoglein 3 cause chronic inflammation [16] anti-matrigel IgG activate the classical pathway [8] anti-HSP70 induce the failure of mucosal immunologic tolerance to HSP70 and develop a mucosal autoimmune response [17] 4. CRS and Human Microbiome 4.1.…”

Section: Autoantibodiesmentioning

confidence: 99%

Autoimmunity: A New Focus on Nasal Polyps

Huang

2023

IJMS

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Chronic rhinosinusitis with nasal polyps (CRSwNP) has long been considered a benign, chronic inflammatory, and hyperplastic disease. Recent studies have shown that autoimmune-related mechanisms are involved in the pathology of nasal polyps. Activated plasma cells, eosinophils, basophils, innate type 2 lymphocytes, mast cells, and proinflammatory cytokine in polyp tissue indicate the mobilization of innate and adaptive immune pathways during polyp formation. The discovery of a series of autoantibodies further supports the autoimmune nature of nasal polyps. Local homeostasis dysregulation, infection, and chronic inflammation may trigger autoimmunity through several mechanisms, including autoantigens overproduction, microbial translocation, molecular mimicry, superantigens, activation or inhibition of receptors, bystander activation, dysregulation of Toll-Like Receptors (TLRs), epitope spreading, autoantigens complementarity. In this paper, we elaborated on the microbiome-mediated mechanism, abnormal host immunity, and genetic changes to update the role of autoimmunity in the pathogenesis of chronic rhinosinusitis with nasal polyps.

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