CD8+ IL-17-producing T cells are important in effector functions for the elicitation of contact hypersensitivity responses.

Academic Article


  • Allergen-induced contact hypersensitivity (CHS) is a T cell-mediated delayed-type immune response which has been considered to be primarily mediated by CD8+ T cytotoxic type I (Tc1) cells. IFN-gamma, the prototype Tc1 (Th1) cytokine, has been implicated as the primary inflammatory cytokine for CHS. In this study, we demonstrate that neutralization of IL-17 rather than IFN-gamma suppresses the elicitation of CHS. The suppression does not result from inhibition of the proliferation of allergen-activated T cells. Allergen sensitization induces the development of distinct CD8+ T cell subpopulations that produce IFN-gamma or IL-17. Although CD8+ IL-17-producing cells are stimulated by IL-23, they are inhibited by IL-12, a prototypical stimulator of IFN-gamma-producing Tc1 cells. This indicates that CD8+ IL-17-producing cells are distinct from Tc1 cells and are important in effector functions at the elicitation of CHS. These studies provide insights into a novel mechanism for CHS.
  • Published In


  • Animals, Antibodies, Monoclonal, CD8-Positive T-Lymphocytes, Cell Migration Inhibition, Dermatitis, Contact, Edema, Female, Haptens, Immunization, Interferon-gamma, Interleukin-17, Leukocytes, Mice, Mice, Inbred C57BL, Skin, T-Lymphocyte Subsets
  • Digital Object Identifier (doi)

    Author List

  • He D; Wu L; Kim HK; Li H; Elmets CA; Xu H
  • Start Page

  • 6852
  • End Page

  • 6858
  • Volume

  • 177
  • Issue

  • 10