Contact hypersensitivity in MHC class II-deficient mice depends on CD8 T lymphocytes primed by immunostimulating...

Studies to determine if CD4+ and/or CD8+ T cells are critical for the initiation and propagation of contact hypersensitivity (CHS) reactions have yielded conflicting results regarding their roles. We studied the induction and expression of CHS to trinitrochlorobenzene (TNCB) using major histocompatibility complex class II-deficient mice that display normal numbers of CD8+ T cells but lack CD4+ T cells. CHS to TNCB, detected as an increase in ear thickness 24 h after epicutaneous challenge, was significantly enhanced in major histocompatibility complex class II-deficient mice compared with wild-type controls. Ear swelling responses in major histocompatibility complex class II-deficient mice were decreased by treatment with anti-CD8 antibody or by injection of wild-type CD4+ T cells. To further characterize mechanisms involved in the initiation of CHS responses, phenotypical and functional characteristics of both freshly isolated and cultured Langerhans cells were studied. Like Langerhans cells from wild-type controls, Langerhans cells from major histocompatibility complex class II-deficient mice upregulated B7-1 and B7-2 costimulatory molecules and enhanced major histocompatibility complex class I expression upon short-term culture. Cultured Langerhans cells induced a 3.5-fold increase in the stimulation of autologous hapten-specific CD8+ T cell proliferation compared with fresh Langerhans cells. Finally, TNP-coupled Langerhans cells from major histocompatibility complex class II-deficient mice primed naive mice to TNCB after transfer. These results demonstrate that hapten-specific CD8+ T cells are sufficient for the expression of CHS and that CD8 priming does not require the presence of CD4+ T cells or major histocompatibility complex class II antigen. Key words: CD8 lymphocytes/MHC class II deficiency.