IL-17 amplifies human contact hypersensitivity by licensing hapten nonspecific Th1 cells to kill autologous keratinocytes

Davide Pennino, Kilian Eyerich, Claudia Scarponi, Teresa Carbone, Stefanie Eyerich, Francesca Nasorri, Simone Garcovich, Claudia Traidl-Hoffmann, Cristina Albanesi, Andrea Cavani

Research output: Contribution to journalArticle

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Abstract

Th17 is a newly identified lineage of effector T cells involved in autoimmunity and immune responses to pathogens. We demonstrate in this study the pathogenic role of IL-17-producing CD4 + T lymphocytes in allergic contact dermatitis (ACD) to skinapplied chemicals. IL-17 + T cells infiltrate ACD reactions and predominantly distribute at the site of heavy spongiosis. Skin IL-17 + T cells were functionally and phenotypically heterogeneous: although pure Th17 prevailed in ACD skin, hapten responsiveness was restricted to Th1/IL-17 (IFN-γ +IL-17 +) and Th0/IL-17 (IFN-γ +IL-17 +IL-4 +) fractions, and to lesser extent Th2/ IL-17 cells. In the IFN-γ-dominated ACD environment, IL-17-releasing T cells affect immune function of keratinocytes by promoting CXCL8, IL-6, and HBD-2 production. In addition, compared with Th1, supernatants from Th1/IL-17 T cells were much more efficient in inducing ICAM-1 expression on keratinocytes and keratinocyte-T cell adhesiveness in vitro. As a consequence, exposure to combined IFN-g and IL-17 rendered keratinocytes susceptible to ICAM-1-dependent Ag non-specific T cell killing. Thus, IL-17 efficiently amplifies the allergic reaction by rendering virtually all of the T lymphocytes recruited at the site of skin inflammation capable to directly contribute to tissue damage.

Original languageEnglish
Pages (from-to)4880-4888
Number of pages9
JournalJournal of Immunology
Volume184
Issue number9
DOIs
Publication statusPublished - May 1 2010

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Th1 Cells
Interleukin-17
Haptens
Contact Dermatitis
Licensure
Keratinocytes
T-Lymphocytes
Allergic Contact Dermatitis
Intercellular Adhesion Molecule-1
Skin
Adhesiveness
Autoimmunity
Interleukin-4
Interleukin-6
Hypersensitivity

ASJC Scopus subject areas

  • Immunology
  • Medicine(all)

Cite this

IL-17 amplifies human contact hypersensitivity by licensing hapten nonspecific Th1 cells to kill autologous keratinocytes. / Pennino, Davide; Eyerich, Kilian; Scarponi, Claudia; Carbone, Teresa; Eyerich, Stefanie; Nasorri, Francesca; Garcovich, Simone; Traidl-Hoffmann, Claudia; Albanesi, Cristina; Cavani, Andrea.

In: Journal of Immunology, Vol. 184, No. 9, 01.05.2010, p. 4880-4888.

Research output: Contribution to journalArticle

Pennino, D, Eyerich, K, Scarponi, C, Carbone, T, Eyerich, S, Nasorri, F, Garcovich, S, Traidl-Hoffmann, C, Albanesi, C & Cavani, A 2010, 'IL-17 amplifies human contact hypersensitivity by licensing hapten nonspecific Th1 cells to kill autologous keratinocytes', Journal of Immunology, vol. 184, no. 9, pp. 4880-4888. https://doi.org/10.4049/jimmunol.0901767
Pennino, Davide ; Eyerich, Kilian ; Scarponi, Claudia ; Carbone, Teresa ; Eyerich, Stefanie ; Nasorri, Francesca ; Garcovich, Simone ; Traidl-Hoffmann, Claudia ; Albanesi, Cristina ; Cavani, Andrea. / IL-17 amplifies human contact hypersensitivity by licensing hapten nonspecific Th1 cells to kill autologous keratinocytes. In: Journal of Immunology. 2010 ; Vol. 184, No. 9. pp. 4880-4888.
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