| First Author | Gerwin N | Year | 1999 |
| Journal | Immunity | Volume | 10 |
| Issue | 1 | Pages | 9-19 |
| PubMed ID | 10023766 | Mgi Jnum | J:54748 |
| Mgi Id | MGI:1335795 | Doi | 10.1016/s1074-7613(00)80002-3 |
| Citation | Gerwin N, et al. (1999) Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2 deficient mice results in extended hyperresponsiveness. Immunity 10(1):9-19 |
| abstractText | ICAM-2-deficient mice exhibit prolonged accumulation of eosinophils in lung interstitium concomitant with a delayed increase in eosinophil numbers in the airway lumen during the develop-ment of allergic lung inflammation. The ICAM-2-dependent increased and prolonged accumulation of eosinophils in lung interstitium results in prolonged, heightened airway hyperresponsiveness. These findings reveal an essential role for ICAM-2 in the development of the inflammatory and respiratory components of allergic lung disease. This phenotype is caused by the lack of ICAM-2 expression on non-hematopoietic cells. ICAM-2 deficiency on endothelial cells causes reduced eosinophil trans-migration in vitro. ICAM-2 is not essential for lymphocyte homing or the development of leukocytes, with the exception of megakaryocyte progenitors, which are significantly reduced. |
