2021
DOI: 10.2340/00015555-3702
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Dermal Periostin: A New Player in Itch of Prurigo Nodularis

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Cited by 28 publications
(18 citation statements)
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“…We recently reported an increased amount of dermal IL‐31 (+) cells, IL‐31Rα (+) cells and epidermal IL‐31Rα expression in lesional PN skin compared to healthy controls that were significantly correlated with itch intensity 21 . Moreover, we found that dermal deposition of periostin is increased in PN lesions compared to healthy controls and is significantly associated with both itch intensity and the amount of dermal IL‐31Ra (+) cells 22 . Altogether, Th2 related immune cells and cytokines likely play a prominent role in both the pathogenesis and pruritus associated with PN.…”
Section: The Role Of the Th2 Immune Response In Chronic Pruritic Cond...mentioning
confidence: 62%
See 1 more Smart Citation
“…We recently reported an increased amount of dermal IL‐31 (+) cells, IL‐31Rα (+) cells and epidermal IL‐31Rα expression in lesional PN skin compared to healthy controls that were significantly correlated with itch intensity 21 . Moreover, we found that dermal deposition of periostin is increased in PN lesions compared to healthy controls and is significantly associated with both itch intensity and the amount of dermal IL‐31Ra (+) cells 22 . Altogether, Th2 related immune cells and cytokines likely play a prominent role in both the pathogenesis and pruritus associated with PN.…”
Section: The Role Of the Th2 Immune Response In Chronic Pruritic Cond...mentioning
confidence: 62%
“…21 Moreover, we found that dermal deposition of periostin is increased in PN lesions compared to healthy controls and is significantly associated with both itch intensity and the amount of dermal IL-31Ra (+) cells. 22 Altogether, Th2 related immune cells and cytokines likely play a prominent role in both the pathogenesis and pruritus associated with PN.…”
Section: Prurigo Nodularismentioning
confidence: 99%
“…A dysregulated Th2-biased immune response is central to the pathogenesis of PN, including cutaneous upregulation of IL-31, IL-4, IL-17, and IL-22 [81,82]. Both pruritogenic alarmins TSLP and periostin are highly expressed in the PN skin and might fuel the itch-scratch cycle via feed-forward amplification loop mechanisms, as discussed previously [82,83]. Increased expression of neuropeptides (substance P, calcitonin gene-related peptide), neurotrophins (nerve growth factor and tropomyosin receptor kinase A receptor) and endothelin, support the notion of a dysregulated neuro-immune-epithelial cross-talk, also explaining the neuronal and epidermal hyperplasia of PN skin [84,85].…”
Section: Prurigo Nodularismentioning
confidence: 90%
“…Another itch mediator associated with the Th2 inflammatory response is extracellular matrix protein, periostin; one study analyzed PN lesions and found that periostin was upregulated in the dermis as well as significantly correlated with itch intensity in these patients. 19 Additional cytokines implicated in the PN immunologic cascade include tryptase, eosinophil cationic protein, histamine, prostaglandins, and neuropeptides. 1 , 3 , 14 , 16 Eosinophil cationic protein and neuropeptides are amongst the granules released by eosinophilic granulocytes, in addition to eosinophil derived neurotoxin, eosinophil protein X, and major basic protein.…”
Section: Introductionmentioning
confidence: 99%