Open AccessInflammatory and immune responses are impaired in mice deficient in intercellular adhesion molecule 1.
Author(s) -
James E. Sligh,
Christie M. Ballantyne,
Susan Solliday Rich,
Hal K. Hawkins,
C. W. Smith,
Allan Bradley,
Arthur L. Beaudet
Publication year - 1993
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.90.18.8529
Subject(s) - granulocytosis , intercellular adhesion molecule 1 , immune system , cell adhesion molecule , biology , immunology , intercellular adhesion molecule , inflammation , mutant , chemokine , microbiology and biotechnology , cell adhesion , granulocyte , cell , gene , genetics
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 beta 2 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.