Abstract | BACKGROUND: OBJECTIVE: To develop a mouse model reflecting nickel allergy in humans induced by epicutaneous exposure to nickel, and to investigate the mechanisms involved in such allergic responses. METHODS: Mice were exposed to NiCl2 on the dorsal side of the ears. Inflammation was evaluated by the swelling and cell infiltration of the ears. T cell responses were determined as numbers of CD4+ and CD8+ T cells in the draining lymph nodes. Localization of nickel was examined by dimethylglyoxime staining. RESULTS: Epicutaneous exposure to nickel results in prolonged localization of nickel in the epidermis, and induces nickel allergy in mice. The allergic response to nickel following epicutaneous exposure is MyD88-dependent and interleukin (IL)-1 receptor-dependent, but independent of toll-like receptor (TLR)-4. CONCLUSION:
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Authors | Marie T Vennegaard, Beatrice Dyring-Andersen, Lone Skov, Morten M Nielsen, Jonas D Schmidt, Michael Bzorek, Steen S Poulsen, Allan R Thomsen, Anders Woetmann, Jacob P Thyssen, Jeanne D Johansen, Niels Odum, Torkil Menné, Carsten Geisler, Charlotte M Bonefeld |
Journal | Contact dermatitis
(Contact Dermatitis)
Vol. 71
Issue 4
Pg. 224-32
(Oct 2014)
ISSN: 1600-0536 [Electronic] England |
PMID | 25040758
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. |
Chemical References |
- Interleukin-1
- Myd88 protein, mouse
- Myeloid Differentiation Factor 88
- Nickel
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Topics |
- Animals
- CD4 Lymphocyte Count
- CD8-Positive T-Lymphocytes
- Dermatitis, Allergic Contact
(immunology, metabolism)
- Disease Models, Animal
- Epidermis
(metabolism)
- Female
- Interleukin-1
(immunology, metabolism)
- Lymphocyte Count
- Mice, Inbred C3H
- Mice, Inbred C57BL
- Mice, Knockout
- Myeloid Differentiation Factor 88
(immunology, metabolism)
- Nickel
(immunology, pharmacokinetics)
- Signal Transduction
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