Nickel allergy is associated with a broad spectrum cytokine response.
IL-5
allergy
contact dermatitis
cytokines
nickel
Journal
Contact dermatitis
ISSN: 1600-0536
Titre abrégé: Contact Dermatitis
Pays: England
ID NLM: 7604950
Informations de publication
Date de publication:
Jan 2023
Jan 2023
Historique:
revised:
14
07
2022
received:
19
04
2022
accepted:
06
08
2022
pubmed:
10
9
2022
medline:
21
12
2022
entrez:
9
9
2022
Statut:
ppublish
Résumé
Nickel-induced proliferation or cytokine release by peripheral blood mononuclear cells may be used for in vitro diagnosis of nickel allergy. Aim of this study was to explore the nickel-specific cytokine profile to further elucidate the pathogenesis of nickel allergic contact dermatitis (ACD) and to identify potential new biomarkers for nickel ACD. Peripheral blood mononuclear cells from patients and controls were cultured with T-cell skewing cytokine cocktails and/or nickel. Cytokine and chemokine concentrations were assessed in culture supernatants using validated multiplex assays. Specific cytokine production was related to history of nickel allergy and patch-test results. Twenty-one of the 33 analytes included in the analysis were associated with nickel allergy and included type1 (TNF-α, IFN-γ, TNF-β), type 2 (IL-3, IL-4, IL-5, IL-13), type 1/2 (IL-2, IL-10), type 9 (IL-9), type 17/1 (IL-17A[F], GM-CSF, IL-21) and type 22 (IL-22) derived cytokines as well as the T-cell/antigen presentation cell derived factors Thymus and activation regulated chemokine (TARC), IL-27 and IP-10. Receiver operator characteristics (ROC) analysis showed that IL-5 was the strongest biomarker for nickel allergy. A broad spectrum of 33 cytokines and chemokines is involved in the allergen-specific immune response in nickel allergic patients. IL-5 remains, next to the lymphocyte proliferation test, the strongest biomarker for nickel allergy.
Sections du résumé
BACKGROUND
BACKGROUND
Nickel-induced proliferation or cytokine release by peripheral blood mononuclear cells may be used for in vitro diagnosis of nickel allergy.
OBJECTIVES
OBJECTIVE
Aim of this study was to explore the nickel-specific cytokine profile to further elucidate the pathogenesis of nickel allergic contact dermatitis (ACD) and to identify potential new biomarkers for nickel ACD.
METHODS
METHODS
Peripheral blood mononuclear cells from patients and controls were cultured with T-cell skewing cytokine cocktails and/or nickel. Cytokine and chemokine concentrations were assessed in culture supernatants using validated multiplex assays. Specific cytokine production was related to history of nickel allergy and patch-test results.
RESULTS
RESULTS
Twenty-one of the 33 analytes included in the analysis were associated with nickel allergy and included type1 (TNF-α, IFN-γ, TNF-β), type 2 (IL-3, IL-4, IL-5, IL-13), type 1/2 (IL-2, IL-10), type 9 (IL-9), type 17/1 (IL-17A[F], GM-CSF, IL-21) and type 22 (IL-22) derived cytokines as well as the T-cell/antigen presentation cell derived factors Thymus and activation regulated chemokine (TARC), IL-27 and IP-10. Receiver operator characteristics (ROC) analysis showed that IL-5 was the strongest biomarker for nickel allergy.
CONCLUSIONS
CONCLUSIONS
A broad spectrum of 33 cytokines and chemokines is involved in the allergen-specific immune response in nickel allergic patients. IL-5 remains, next to the lymphocyte proliferation test, the strongest biomarker for nickel allergy.
Identifiants
pubmed: 36082421
doi: 10.1111/cod.14199
pmc: PMC10087880
doi:
Substances chimiques
Nickel
7OV03QG267
Cytokines
0
Interleukin-5
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
10-17Subventions
Organisme : TTW
Informations de copyright
© 2022 The Authors. Contact Dermatitis published by John Wiley & Sons Ltd.
Références
J Leukoc Biol. 2000 Jun;67(6):757-66
pubmed: 10857846
Clin Exp Immunol. 2006 Dec;146(3):417-26
pubmed: 17100760
J Eur Acad Dermatol Venereol. 2018 Sep;32(9):1542-1548
pubmed: 29524267
J Invest Dermatol. 2014 Jul;134(7):1903-1911
pubmed: 24487305
Nat Immunol. 2010 Sep;11(9):814-9
pubmed: 20711192
Scand J Immunol. 2005 Sep;62(3):289-96
pubmed: 16179016
Clin Exp Allergy. 2004 Sep;34(9):1458-66
pubmed: 15347381
Br J Dermatol. 2004 Jul;151(1):32-41
pubmed: 15270870
Clin Exp Immunol. 1988 Dec;74(3):387-91
pubmed: 2976621
J Allergy Clin Immunol. 2009 Feb;123(2):486-92
pubmed: 18986691
Contact Dermatitis. 2015 May;72(5):286-96
pubmed: 25580524
Curr Opin Allergy Clin Immunol. 2020 Aug;20(4):367-373
pubmed: 32590505
Br J Dermatol. 2017 Jun;176(6):1533-1540
pubmed: 28382616
Clin Exp Allergy. 2020 Jun;50(6):722-732
pubmed: 32215995
F1000Res. 2018 Jun 20;7:
pubmed: 29983912
Curr Opin Allergy Clin Immunol. 2006 Oct;6(5):340-4
pubmed: 16954787
Contact Dermatitis. 2007 Feb;56(2):63-9
pubmed: 17244072
Contact Dermatitis. 2004 May;50(5):304-12
pubmed: 15209812
J Immunol. 2008 Feb 1;180(3):1471-81
pubmed: 18209042
Chem Res Toxicol. 2018 Dec 17;31(12):1323-1331
pubmed: 30421605
Arch Dermatol Res. 2000 Jun;292(6):285-91
pubmed: 10929769
Int Arch Allergy Immunol. 2003 Dec;132(4):373-9
pubmed: 14707469
Contact Dermatitis. 2023 Jan;88(1):10-17
pubmed: 36082421
An Bras Dermatol. 2018 Nov/Dec;93(6):829-835
pubmed: 30484527
Clin Exp Immunol. 2006 Mar;143(3):494-502
pubmed: 16487249
Contact Dermatitis. 2013 Jun;68(6):339-47
pubmed: 23692034
J Invest Dermatol. 2017 Oct;137(10):2140-2148
pubmed: 28634033
Exp Dermatol. 2007 Dec;16(12):1032-40
pubmed: 18031463
Exp Dermatol. 2005 Aug;14(8):634-40
pubmed: 16026586