Journal article
Authors list: Rafei-Shamsabadi, David A.; van de Poel, Saskia; Dorn, Britta; Kunz, Stefanie; Martin, Stefan F.; Klose, Christoph S. N.; Arnold, Sebastian J.; Tanriver, Yakup; Ebert, Karolina; Diefenbach, Andreas; Halim, Timotheus Y. F.; McKenzie, Andrew N. J.; Jakob, Thilo
Publication year: 2018
Pages: 1962-1972
Journal: Journal of Investigative Dermatology
Volume number: 138
Issue number: 9
ISSN: 0022-202X
eISSN: 1523-1747
Open access status: Hybrid
DOI Link: https://doi.org/10.1016/j.jid.2018.03.001
Publisher: Elsevier
Abstract:
Allergic contact dermatitis and its animal model, contact hypersensitivity, are T-cell-mediated inflammatory skin diseases that require activation of the innate immune system. Here we investigate the role of innate lymphoid cells (ILCs) during the elicitation phase of 2,4,6-trinitrochlorobenzene-induced contact hypersensitivity using Eomes(Gfp/+) x Rorc(gamma t)-Cre(Tg) x Rosa26R(Yfp/+) reporter mice. Ear swelling responses, cutaneous ILC numbers, and cytokine production were determined at different time points. Functional analyses were performed in a CD90.1/.2 congenic adoptive transfer model that allowed selective antibody-mediated depletion of ILCs before hapten challenge, and in Rora(sg/flox)Il7r(Cre/+) mice, which lack ILC2. Hapten challenge induced early increases of natural killer cells in skin and ear draining lymph nodes corresponding to the peak ear swelling response. In contrast, ILC1, 2, and 3 showed a delayed increase in numbers corresponding to the contact hypersensitivity resolution phase. Hapten challenge induced increased marker cytokines in all ILC subtypes and an activated phenotype in ILC2. Depletion of all ILC resulted in a significantly enhanced ear swelling response. Similarly, ILC2-deficient mice (Rora(sg/flox)Il7r(Cre/+)) displayed increased ear swelling responses on hapten challenge, suggesting that ILC2 act as negative regulators in the type 1-dominated immune response of contact hypersensitivity.
Citation Styles
Harvard Citation style: Rafei-Shamsabadi, D., van de Poel, S., Dorn, B., Kunz, S., Martin, S., Klose, C., et al. (2018) Lack of Type 2 Innate Lymphoid Cells Promotes a Type I-Driven Enhanced Immune Response in Contact Hypersensitivity, Journal of Investigative Dermatology, 138(9), pp. 1962-1972. https://doi.org/10.1016/j.jid.2018.03.001
APA Citation style: Rafei-Shamsabadi, D., van de Poel, S., Dorn, B., Kunz, S., Martin, S., Klose, C., Arnold, S., Tanriver, Y., Ebert, K., Diefenbach, A., Halim, T., McKenzie, A., & Jakob, T. (2018). Lack of Type 2 Innate Lymphoid Cells Promotes a Type I-Driven Enhanced Immune Response in Contact Hypersensitivity. Journal of Investigative Dermatology. 138(9), 1962-1972. https://doi.org/10.1016/j.jid.2018.03.001
Keywords
DERMATITIS; NATURAL-KILLER