title: T cells reactive to keratinocyte antigens are generated during induction of contact hypersensitivity in mice. A model for autoeczematization in humans?
abstract: BACKGROUND
  The role of keratinocytes (KC) in contact hypersensitivity (CH) has been examined more with respect to cytokine secretion and tolerance induction and less as a source of antigenic proteins to which chemical haptens can conjugate.
  
  
  OBJECTIVE
  To determine whether KC-derived proteins can serve as antigenic carriers for haptens such as dinitrofluorobenzene (DNFB).
  
  
  METHODS
  We examined the capacity of draining lymph node cells from BALB/c mice sensitized to DNFB to proliferate in response to hapten or to hapten-conjugated protein extracts derived from a KC line (DNP-Pam KC extract). Using limiting dilution microculture of these lymph node cells, we established DNP-specific T cell clones as well as DNP-Pam KC extract-reactive T cell clones. We also examined the proliferative responses of the DNP-Pam KC extract-reactive clones and of lymph node cells from mice sensitized to different haptens.
  
  
  RESULTS
  Lymph node cells from DNFB-sensitized mice proliferated well to hapten or to DNP-Pam KC extract. Six la(d)-restricted, alphabeta TCR-bearing, CD4+ clones were established: 4 proliferated specifically to soluble hapten (DNBS), whereas 2 proliferated in response to DNP-Pam KC extract. Surprisingly, the DNP-Pam KC extract-reactive clones proliferated as well to Pam KC extract without hapten. Lymph node cells from hapten-sensitized mice not only proliferated specifically in response to the hapten to which they were sensitized, but also proliferated to Pam KC extract without hapten.
  
  
  CONCLUSIONS
  T cell clones generated during the induction of (CH) in mice include those reactive to hapten as well as those reactive to KC antigens independent of hapten. Analogous mechanisms in humans might account for autoreactive events such as id reactions associated with CH and angry back syndrome during patch testing.
authors.affiliation: Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9069, USA.
authors.forename: B S
authors.initials: BS
authors.lastname: Fehr
authors.forename: A
authors.initials: A
authors.lastname: Takashima
authors.forename: P R
authors.initials: PR
authors.lastname: Bergstresser
authors.forename: P D
authors.initials: PD
authors.lastname: Cruz
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology*; D001327:Autoimmune Diseases / Q000276:immunology*; D016207:Cytokines / Q000276:immunology; D003877:Dermatitis, Contact / Q000209:etiology / Q000276:immunology*; D004139:Dinitrofluorobenzene; D004195:Disease Models, Animal; D004485:Eczema / Q000139:chemically induced / Q000276:immunology*; D005260:Female; D006241:Haptens / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D015603:Keratinocytes / Q000276:immunology*; D008208:Lymphatic System / Q000166:cytology* / Q000276:immunology*; D051379:Mice; D008806:Mice, Inbred AKR; D008807:Mice, Inbred BALB C; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000941:Antigens; D016207:Cytokines; D006241:Haptens; D004139:Dinitrofluorobenzene