Characterization of the altered cutaneous reactivity of transgenic mice whose keratinocytes overexpress B7-1

Clin Immunol Immunopathol. 1998 Mar;86(3):259-70. doi: 10.1006/clin.1997.4491.

Abstract

B7-1 (CD80) is a second signal molecule usually associated with "professional" APCs that prevents the induction of T-cell clonal anergy and induces IL-2 production during antigen presentation. Tg mice whose epidermal KC overexpress B7-1 exhibit exaggerated and persistent CHS to a variety of haptens that lasts up to 8 weeks after hapten challenge. These Tg mice also exhibit significantly enhanced ear-swelling responses to irritants that are not persistent. Exaggerated CHS was not reflected in the draining lymph node. T-lymphocyte proliferative responses after sensitization and local challenge with haptens, as there were no significant differences between the B7-1 Tg and the NTg mice. However, RT-PCR analysis of mouse ear skin at the hapten challenge site indicated that B7-1 Tg mice had an alteration in the kinetics of in situ lymphokine transcripts compared to NTg mice: IFN-gamma transcripts were first detectable in Tg mouse skin at 2 weeks versus 24 h for NTg mice. RNase protection assays to detect inflammatory cytokine transcripts at hapten application sites indicated that B7-1 Tg mice responded to hapten application with increased TNF-alpha, IL-6, and TNF-beta transcripts compared to NTg mice. Thus, hapten-induced ear swelling in these Tg mice may be mediated by enhanced inflammatory cytokines during the early phase (1-14 days). IFN-gamma-producing lymphocytes may be responsible for the late phase of the ear-swelling response (14-42 days). These data indicate that B7-1 overexpression by KC in mouse skin directly or indirectly affects the nature of cutaneous inflammation induced by haptens and irritants.

MeSH terms

  • Animals
  • B7-1 Antigen / genetics*
  • Base Sequence
  • Cytokines / metabolism
  • DNA Primers / genetics
  • Dermatitis, Contact / genetics
  • Dermatitis, Contact / immunology
  • Dermatitis, Contact / pathology
  • Gene Expression
  • Haptens / administration & dosage
  • In Vitro Techniques
  • Inflammation / etiology
  • Inflammation / immunology
  • Inflammation Mediators / metabolism
  • Keratinocytes / immunology*
  • Kinetics
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred DBA
  • Mice, Transgenic
  • Polymerase Chain Reaction
  • Skin / immunology*
  • T-Lymphocytes / immunology

Substances

  • B7-1 Antigen
  • Cytokines
  • DNA Primers
  • Haptens
  • Inflammation Mediators