Inflammatory and immune responses are impaired in mice deficient in intercellular adhesion molecule 1

James E. Sligh, Christie M. Ballantyne, Susan S. Rich, Hal K. Hawkins, C. Wayne Smith, Allan Bradley, Arthur L. Beaudet

Research output: Contribution to journalArticlepeer-review

529 Scopus citations


Gene targeting was used to produce mice deficient in intercellular adhesion molecule 1 (ICAM-1) or CD54, an immunoglobulin-like cell adhesion molecule that binds β2 integrins. Homozygous deficient animals develop normally, are fertile, and have a moderate granulocytosis. The nature of the mutation, RNA analysis, and immunostaining are consistent with complete loss of surface expression of ICAM-1. Deficient mice exhibit prominent abnormalities of inflammatory responses including impaired neutrophil emigration in response to chemical peritonitis and decreased contact hypersensitivity to 2,4-dinitrofluorobenzene. Mutant cells provided negligible stimulation in the mixed lymphocyte reaction, although they proliferated normally as responder cells. These mutant animals will be extremely valuable for examining the role of ICAM-1 and its counterreceptors in inflammatory disease processes and atherosclerosis.

Original languageEnglish (US)
Pages (from-to)8529-8533
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number18
StatePublished - Sep 15 1993
Externally publishedYes


  • Cell adhesion
  • Gene targeting
  • Homologous recombination
  • Immune deficiency
  • Lymphocyte interactions

ASJC Scopus subject areas

  • General
  • Genetics


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