Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2-deficient mice results in extended hyperresponsiveness

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 development of allergic lung inflammation. The ICAM-2-dependent increased and prolonged accumulation of eosinophils in lun g interstitium results in prolonged, heightened airway hyperresponsiveness. These findings reveal an essential role for ICAM-2 in the development of t he inflammatory and respiratory components of allergic lung disease. This p henotype is caused by the lack of ICAM-2 expression on non-hematopoietic ce lls. ICAM-2 deficiency on endothelial cells causes reduced eosinophil trans migration in vitro. ICAM-2 is not essential for lymphocyte homing or the de velopment of leukocytes, with the exception of megakaryocyte progenitors, w hich are significantly reduced.