@article {528331, title = {Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2 deficient mice results in extended hyperresponsiveness}, journal = {Immunity}, volume = {10}, number = {1}, year = {1999}, note = {Reprint Status: NOT In File}, pages = {9-19}, abstract = {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 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 transmigration 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.}, author = {Gerwin,N. and Gonzalo,J.A. and Lloyd,C. and Coyle,A.J. and Reiss,Y. and Banu,N. and Wang, B. and Xu, H and Avraham,H. and Engelhardt,B. and Springer, T.A. and Gutierrez-Ramos,J.C.} }