IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis. / Larsen, Jeppe Madura; Bonefeld, Charlotte Menné; Poulsen, Steen Seier; Geisler, Carsten; Skov, Lone.

In: Journal of Allergy and Clinical Immunology, Vol. 123, No. 2, 2009, p. 486-92.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Larsen, JM, Bonefeld, CM, Poulsen, SS, Geisler, C & Skov, L 2009, 'IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis', Journal of Allergy and Clinical Immunology, vol. 123, no. 2, pp. 486-92. https://doi.org/10.1016/j.jaci.2008.09.036

APA

Larsen, J. M., Bonefeld, C. M., Poulsen, S. S., Geisler, C., & Skov, L. (2009). IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis. Journal of Allergy and Clinical Immunology, 123(2), 486-92. https://doi.org/10.1016/j.jaci.2008.09.036

Vancouver

Larsen JM, Bonefeld CM, Poulsen SS, Geisler C, Skov L. IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis. Journal of Allergy and Clinical Immunology. 2009;123(2):486-92. https://doi.org/10.1016/j.jaci.2008.09.036

Author

Larsen, Jeppe Madura ; Bonefeld, Charlotte Menné ; Poulsen, Steen Seier ; Geisler, Carsten ; Skov, Lone. / IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis. In: Journal of Allergy and Clinical Immunology. 2009 ; Vol. 123, No. 2. pp. 486-92.

Bibtex

@article{5b089f0096cc11de8bc9000ea68e967b,
title = "IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis",
abstract = "BACKGROUND: IL-17-producing T(H) (T(H)17) cells are key mediators of chronic inflammation in mice. Recent studies have implicated T(H)17-mediated inflammation in the pathogenesis of human autoimmune diseases; however, the involvement of T(H)17 cells in allergic disorders remains largely elusive. OBJECTIVE: To investigate T(H)17-mediated inflammation in human beings with allergic contact dermatitis; in particular, the innate response of keratinocytes to contact allergen, the induction of allergen-specific T(H)17 cells, and the presence of T(H)17-related effector cells in inflamed skin. METHODS: Human keratinocytes were stimulated with nickel in vitro followed by measurements of IL-23 and IL-12 production by quantitative PCR and ELISA. Allergen-specific memory T cells from the blood of individuals with nickel allergy and healthy controls were identified and characterized by using a short-term ex vivo assay. Nickel patch test lesions and normal skin were analyzed for the expression of T(H)17-related cells and molecules by using immunohistochemistry. RESULTS: Keratinocytes were found to produce IL-23, but no detectable IL-12, in a response to nickel stimulation. Memory T cells isolated from peripheral blood of individuals with nickel allergy, but not healthy controls, contained T(H)17 and T(H)1 cells proliferating in response to nickel-pulsed DCs. Inflamed skin of nickel-challenged allergic individuals contained infiltrating neutrophils and cells expressing IL-17, IL-22, CCR6, and IL-22R. CONCLUSION: Our results demonstrate the involvement of T(H)17-mediated immunopathology in human allergic contact dermatitis, including both innate and adaptive immune responses to contact allergens.",
author = "Larsen, {Jeppe Madura} and Bonefeld, {Charlotte Menn{\'e}} and Poulsen, {Steen Seier} and Carsten Geisler and Lone Skov",
note = "Keywords: Allergens; Cell Proliferation; Cells, Cultured; Dermatitis, Allergic Contact; Humans; Inflammation; Interleukin-12; Interleukin-17; Interleukin-23; Interleukins; Keratinocytes; Nickel; Receptors, CCR6; Receptors, Interleukin; T-Lymphocytes, Helper-Inducer",
year = "2009",
doi = "10.1016/j.jaci.2008.09.036",
language = "English",
volume = "123",
pages = "486--92",
journal = "Journal of Allergy and Clinical Immunology",
issn = "0091-6749",
publisher = "Mosby Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - IL-23 and T(H)17-mediated inflammation in human allergic contact dermatitis

AU - Larsen, Jeppe Madura

AU - Bonefeld, Charlotte Menné

AU - Poulsen, Steen Seier

AU - Geisler, Carsten

AU - Skov, Lone

N1 - Keywords: Allergens; Cell Proliferation; Cells, Cultured; Dermatitis, Allergic Contact; Humans; Inflammation; Interleukin-12; Interleukin-17; Interleukin-23; Interleukins; Keratinocytes; Nickel; Receptors, CCR6; Receptors, Interleukin; T-Lymphocytes, Helper-Inducer

PY - 2009

Y1 - 2009

N2 - BACKGROUND: IL-17-producing T(H) (T(H)17) cells are key mediators of chronic inflammation in mice. Recent studies have implicated T(H)17-mediated inflammation in the pathogenesis of human autoimmune diseases; however, the involvement of T(H)17 cells in allergic disorders remains largely elusive. OBJECTIVE: To investigate T(H)17-mediated inflammation in human beings with allergic contact dermatitis; in particular, the innate response of keratinocytes to contact allergen, the induction of allergen-specific T(H)17 cells, and the presence of T(H)17-related effector cells in inflamed skin. METHODS: Human keratinocytes were stimulated with nickel in vitro followed by measurements of IL-23 and IL-12 production by quantitative PCR and ELISA. Allergen-specific memory T cells from the blood of individuals with nickel allergy and healthy controls were identified and characterized by using a short-term ex vivo assay. Nickel patch test lesions and normal skin were analyzed for the expression of T(H)17-related cells and molecules by using immunohistochemistry. RESULTS: Keratinocytes were found to produce IL-23, but no detectable IL-12, in a response to nickel stimulation. Memory T cells isolated from peripheral blood of individuals with nickel allergy, but not healthy controls, contained T(H)17 and T(H)1 cells proliferating in response to nickel-pulsed DCs. Inflamed skin of nickel-challenged allergic individuals contained infiltrating neutrophils and cells expressing IL-17, IL-22, CCR6, and IL-22R. CONCLUSION: Our results demonstrate the involvement of T(H)17-mediated immunopathology in human allergic contact dermatitis, including both innate and adaptive immune responses to contact allergens.

AB - BACKGROUND: IL-17-producing T(H) (T(H)17) cells are key mediators of chronic inflammation in mice. Recent studies have implicated T(H)17-mediated inflammation in the pathogenesis of human autoimmune diseases; however, the involvement of T(H)17 cells in allergic disorders remains largely elusive. OBJECTIVE: To investigate T(H)17-mediated inflammation in human beings with allergic contact dermatitis; in particular, the innate response of keratinocytes to contact allergen, the induction of allergen-specific T(H)17 cells, and the presence of T(H)17-related effector cells in inflamed skin. METHODS: Human keratinocytes were stimulated with nickel in vitro followed by measurements of IL-23 and IL-12 production by quantitative PCR and ELISA. Allergen-specific memory T cells from the blood of individuals with nickel allergy and healthy controls were identified and characterized by using a short-term ex vivo assay. Nickel patch test lesions and normal skin were analyzed for the expression of T(H)17-related cells and molecules by using immunohistochemistry. RESULTS: Keratinocytes were found to produce IL-23, but no detectable IL-12, in a response to nickel stimulation. Memory T cells isolated from peripheral blood of individuals with nickel allergy, but not healthy controls, contained T(H)17 and T(H)1 cells proliferating in response to nickel-pulsed DCs. Inflamed skin of nickel-challenged allergic individuals contained infiltrating neutrophils and cells expressing IL-17, IL-22, CCR6, and IL-22R. CONCLUSION: Our results demonstrate the involvement of T(H)17-mediated immunopathology in human allergic contact dermatitis, including both innate and adaptive immune responses to contact allergens.

U2 - 10.1016/j.jaci.2008.09.036

DO - 10.1016/j.jaci.2008.09.036

M3 - Journal article

C2 - 18986691

VL - 123

SP - 486

EP - 492

JO - Journal of Allergy and Clinical Immunology

JF - Journal of Allergy and Clinical Immunology

SN - 0091-6749

IS - 2

ER -

ID: 14119328