| First Author | Sligh JE Jr | Year | 1993 |
| Journal | Proc Natl Acad Sci U S A | Volume | 90 |
| Issue | 18 | Pages | 8529-33 |
| PubMed ID | 8104338 | Mgi Jnum | J:14565 |
| Mgi Id | MGI:62730 | Doi | 10.1073/pnas.90.18.8529 |
| Citation | Sligh JE Jr, et al. (1993) Inflammatory and immune responses are impaired in mice deficient in intercellular adhesion molecule 1. Proc Natl Acad Sci U S A 90(18):8529-33 |
| abstractText | 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. |
