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Gerwin, N. et al.

Gerwin, Gonzalo, Lloyd, Coyle, Reiss, Banu, Wang, Xu, Avraham, Engelhardt, Springer, Gutierrez-Ramos,

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 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.[1]

References

Prolonged eosinophil accumulation in allergic lung interstitium of ICAM-2 deficient mice results in extended hyperresponsiveness. Gerwin, N., Gonzalo, J.A., Lloyd, C., Coyle, A.J., Reiss, Y., Banu, N., Wang, B., Xu, H., Avraham, H., Engelhardt, B., Springer, T.A., Gutierrez-Ramos, J.C. Immunity (1999) [Pubmed]

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