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    Immunity. 1999 Jan;10(1):9-19.

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

    Gerwin N, Gonzalo JA, Lloyd C, Coyle AJ, Reiss Y, Banu N, Wang B, Xu H, Avraham H, Engelhardt B, Springer TA, Gutierrez-Ramos JC.

    Source

    Millennium Biotherapeutics, Cambridge, Massachusetts 02139, USA. gerwin@mpi.com

    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.

    PMID:
    10023766
    [PubMed - indexed for MEDLINE]

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