title: Diminished contact hypersensitivity response in IL-4 deficient mice at a late phase of the elicitation reaction.
abstract: Contact hypersensitivity (CHS) is thought to depend on the activation of T cells of Th1 and/or Tc1 type. The role of Th2/Tc2 cells in the contact allergic reaction is not clear. The aim of this study was to analyse the functional contribution of Th2/Tc2 cells in CHS using the interleukin-4 (IL-4) deficient mouse model. Interleukin-4 deficient (IL4T) and control (wt) mice were sensitized by epicutaneous application of 2,4-dinitrofluorobenzene. The ear swelling response measured 24 h after challenge was similar in IL4T and control mice. However, from 48 h onwards, ear swelling values were significantly reduced in IL4T mice. The stimulatory capacity of freshly isolated as well as 3-day cultured epidermal cells, prepared from IL4T and wt mice, for allogeneic T cells in a primary and secondary response, was comparable. The reduced number of T cell receptor (TCR) gamma delta+ cells observed in epidermal sheets prepared from IL4T mice was not responsible for the decreased ear swelling response in IL4T mice, because the use of TCR delta deficient mice lacking TCR gamma delta+ cells revealed a down-regulatory role of this cell population in the CHS response. The data indicate that the effector stage of the CHS response can be subdivided into two phases. The first phase proceeds efficiently in IL-4 deficient mice indicating the dependence on Th1/Tc1 cells, while the second phase does not develop in mice lacking IL-4, suggesting the possibility that Th2/Tc2 cells intensify the reaction.
authors.affiliation: Department of Dermatology, Johannes Gutenberg-University, Mainz, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Weigmann
authors.forename: J
authors.initials: J
authors.lastname: Schwing
authors.forename: H
authors.initials: H
authors.lastname: Huber
authors.forename: R
authors.initials: R
authors.lastname: Ross
authors.forename: H
authors.initials: H
authors.lastname: Mossmann
authors.forename: J
authors.initials: J
authors.lastname: Knop
authors.forename: A B
authors.initials: AB
authors.lastname: Reske-Kunz
mesh_terms: D000818:Animals; D002452:Cell Count; D003713:Dendritic Cells / Q000473:pathology; D003877:Dermatitis, Contact / Q000209:etiology / Q000235:genetics* / Q000276:immunology*; D004817:Epidermis / Q000276:immunology / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D015847:Interleukin-4 / Q000172:deficiency*; D007801:Langerhans Cells / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000502:physiology; D012867:Skin / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000473:pathology
chemical_list: D016692:Receptors, Antigen, T-Cell, gamma-delta; D015847:Interleukin-4