{ event: "article_read", name: `Type 2 Inflammation may play a role in Prurigo Nodularis Pathophysiology1`, author: ``, tags: `Prurigo Nodularis`, publication_date: ``, interaction_type: "content" }
Type 2 Inflammation may play a role in Prurigo Nodularis Pathophysiology1
Exact pathophysiology of PN is currently not understood. Based on the evolving literature, type 2 inflammation may play a role in PN.
PN lesions contain a number of immune cells, including type 2 cells1-8
Th2 cells, Th17 cells, and Th22 cells
Macrophages
Eosinophils
Mast cells
Basophils
Increased activity of type 2 cytokines IL-4, IL-13, and IL-31, as well as other inflammatory mediators (IL-17, IL-22, pruritogens, and neuropeptides), is present in PN skin4,5,9,10
IL-4
IL-13
IL-31
Signaling of type 2 cytokines, including IL-4 and IL-13, may contribute to signs and symptoms of PN
IL-4, IL-13, and IL-31 potential effects on itch
Sensitization of nerves to pruritogens11,a
Upregulation of the receptor for IL-3112,13
IL-4, IL-13, and IL-31 potential effects on skin
Increased fibroblast proliferation and collagen production,periostin expression and stimulating profibrotic cytokine TGF-β production may influence skin remodeling and nodule formation11,12
Skin barrier dysfunction: inhibition of keratinocyte differentiation and altered lipid synthesis13
Epidermal differentiation, inflammatory responses, and extracellular remodeling14
The skin, immune system, and nervous system have a dysregulated relationship in PN15-19
Increased activity of type 2 immune cells and cytokines, along with certain other immune cells and inflammatory mediators, may contribute to signs and symptoms of PN through interactions with neurons and other dermal and epidermal resident cells1-10,20-23
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