Role for Id-1 in immunobiology of normal keratinocytes and in basal cell carcinoma

Vijaya Chaturvedi, Brian Bonish, Patricia Bacon, Jian Zhong Qin, Mitchell F. Denning, Kimberly Foreman, Manuel O. Diaz, June Robinson, Brian J. Nickoloff*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


It has been established that Id proteins can block the basic helix-loop-helix (HLH) transcription factors, thereby impacting the onset of senescence in keratinocytes, as well as influencing tumorigenesis involving squamous cell carcinomas. However, the ability of Id-1 to influence the immunologic response of epithelial cells to cytokines implicated in cutaneous oncology such as gamma interferon (IFN-γ) has not been determined. Using a whole population of human keratinocytes infected with a retrovirus to induce over-expression of Id-1, the influence on early differentiation of rapidly proliferating keratinocytes was assessed, as was the response to IFN-γ. While induction of involucrin, a marker of early differentiation, was not altered in Id-1 overexpressing keratinocytes, the IFN-γ mediated increase in intercellular adhesion molecule-1 (ICAM-1) and HLA-DR was reduced. No change in constitutive or inducible levels of MHC class I antigen, CD95 (Fas antigen) or LFA-3 (CD58) was observed in this system. Immunostaining and Western blot analysis revealed over-expression of Id-1 in basal cell carcinomas (BCCs). These tumors not only strongly and diffusely expressed Id-1, but were also characterized by reduced ICAM-1 and HLA-DR expression. Thus, dysregulated Id-1 may not only contribute to delaying the senescence program in keratinocytes, it may also contribute to the escape of the relatively undifferentiated tumor cells in BCC from immune surveillance.

Original languageEnglish (US)
Pages (from-to)255-260
Number of pages6
JournalExperimental Dermatology
Issue number3
StatePublished - Jun 2003


  • Adhesion molecules
  • Differentiation
  • Id-1
  • Immubiology
  • Skin cancer

ASJC Scopus subject areas

  • Dermatology
  • Molecular Biology
  • Biochemistry


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