| First Author | Ramos TN | Year | 2013 |
| Journal | J Biol Chem | Volume | 288 |
| Issue | 16 | Pages | 10962-6 |
| PubMed ID | 23493396 | Mgi Jnum | J:325799 |
| Mgi Id | MGI:6872709 | Doi | 10.1074/jbc.C113.457028 |
| Citation | Ramos TN, et al. (2013) Experimental cerebral malaria develops independently of endothelial expression of intercellular adhesion molecule-1 (icam-1). J Biol Chem 288(16):10962-6 |
| abstractText | Cerebral malaria (CM) is a severe clinical complication of Plasmodium falciparum malaria infection and is characterized by a high fatality rate and neurological damage. Sequestration of parasite-infected red blood cells in brain microvasculature utilizes host- and parasite-derived adhesion molecules and is an important factor in the development of CM. ICAM-1, an alternatively spliced adhesion molecule, is believed to be critical on endothelial cells for infected red blood cell sequestration in CM. Using ICAM-1 mutant mice, we found that the full-length ICAM-1 isoform is not required for development of murine experimental CM (ECM) and that ECM phenotype varies with the combination of ICAM-1 isoforms expressed. Furthermore, we observed development of ECM in transgenic mice expressing ICAM-1 only on leukocytes, indicating that endothelial cell expression of this adhesion molecule is not required for disease pathogenesis. We propose that ICAM-1-dependent cellular aggregation, independent of ICAM-1 expression on the cerebral microvasculature, contributes to ECM. |
