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

JE Sligh Jr, CM Ballantyne, SS Rich… - Proceedings of the …, 1993 - National Acad Sciences
JE Sligh Jr, CM Ballantyne, SS Rich, HK Hawkins, CW Smith, A Bradley, AL Beaudet
Proceedings of the National Academy of Sciences, 1993National Acad Sciences
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 …
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.
National Acad Sciences