Interleukin-36 cytokines are overexpressed in the skin and sera of patients with bullous pemphigoid.
bullous pemphigoid
interleukin-36
interleukin-36 receptor antagonist
interleukin-38
psoriasis
Journal
Experimental dermatology
ISSN: 1600-0625
Titre abrégé: Exp Dermatol
Pays: Denmark
ID NLM: 9301549
Informations de publication
Date de publication:
06 2023
06 2023
Historique:
revised:
21
02
2023
received:
19
12
2022
accepted:
28
02
2023
medline:
9
6
2023
pubmed:
21
3
2023
entrez:
20
3
2023
Statut:
ppublish
Résumé
Bullous pemphigoid (BP) is an autoimmune bullous disease, characterized by autoantibodies targeting BP180 and BP230. The role of interleukin (IL)-36, a potent chemoattractant for granulocytes, in BP remains elusive.The expression of IL-36 cytokines (IL-36α, β, γ) and their antagonists (IL-36Ra and IL-38) was analysed in the skin and serum samples of patients with BP (n = 31), psoriasis (n = 10) and healthy controls (HC) (n = 14) by quantitative polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Skin and serum levels of all cytokines were correlated with the Bullous Pemphigoid Disease Area Index (BPDAI) score and with the serum concentration of pathogenic antibodies.IL-36α, IL-36β, IL-36γ and IL-36Ra were significantly (p < 0.05) overexpressed in BP skin compared to HC, without remarkable differences relative to psoriasis skin. The expression of IL-38 was significantly (p < 0.05) higher in BP compared to psoriasis skin.IL-36α and γ, but not β, serum concentrations were significantly (p < 0.05) higher in BP compared to HC. IL-36γ was significantly (p < 0.05) more expressed in the serum of psoriasis patients than BP. The serum concentration of IL-36Ra and IL-38 were similar between BP and HC, while IL-38 serum levels were significantly (p < 0.05) higher in BP compared to psoriasis patients. Serum IL-36α correlated significantly with BPDAI (r = 0.5 p = 0.001).IL-36 agonists are increased in BP patients, both locally and systemically. Serum IL-36α might represent a potential biomarker for BP. An inefficient balance between IL-36 agonists and antagonists is likely to occur during BP inflammation.
Substances chimiques
Cytokines
0
Interleukins
0
Autoantibodies
0
Autoantigens
0
Non-Fibrillar Collagens
0
IL-38 protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
915-921Informations de copyright
© 2023 The Authors. Experimental Dermatology published by John Wiley & Sons Ltd.
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