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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0607347

Received for publication June 4, 2007.
Revised March 20, 2008.
Accepted for publication March 24, 2008.

Article

An eosinophil immune response characterizes the inflammatory skin disease observed in Tie-2 transgenic mice

Daniel Voskas *{dagger}, Yael Babichev *{dagger}, Ling S. Ling *{dagger}, Jennifer Alami {dagger}, Yuval Shaked {dagger}, Robert S. Kerbel *{dagger}{ddagger}, Brian Ciruna {sect}, and Daniel J. Dumont *{dagger}{ddagger}@

Departments of *Medical Biophysics and {sect}Molecular & Medical Genetics, University of Toronto, Toronto, Ontario, Canada; {dagger}Division of Molecular and Cellular Biology, Sunnybrook Research Institute, Toronto, Ontario, Canada; {ddagger}Toronto-Sunnybrook Regional Cancer Centre, Toronto, Ontario, Canada; and Department of Developmental & Stem Cell Biology, Hospital for Sick Children, Toronto, Ontario, Canada

@ To whom correspondence should be addressed. E-mail: dan.dumont{at}sri.ca.


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Abstract

Although mouse models of inflammatory skin diseases such as psoriasis and atopic dermatitis fail to completely phenocopy disease in humans, they provide invaluable tools to examine the molecular and cellular mechanisms responsible for the epidermal hyperplasia, inflammation, and excess angiogenesis observed in human disease. We have previously characterized a tyrosine kinase with Ig and epidermal growth factor homology domain-2 (Tie-2) transgenic mouse model of an inflammatory skin disease exhibiting these features. More specifically, we demonstrated that the inflammatory component consisted of increased infiltration of CD3-positive T lymphocytes and mast cells in the skin. Here, we further characterize the inflammatory component in the blood and skin of Tie-2 transgenic mice at cellular and molecular levels. We observed increased numbers of CD3-positive T lymphocytes in the blood and increased infiltration of eosinophils in the skin. Furthermore, we characterized cytokine protein and gene expression in the blood and skin, respectively, and observed the deregulated expression of cytokines associated with Th1 and eosinophil immune responses. Interestingly, treatment of Tie-2 transgenic mice with anti-CD4 antibody appeared to resolve aspects of inflammation but did not resolve epidermal hyperplasia, suggesting an important role for eosinophils in mediating the inflammatory skin disease observed in Tie-2 transgenic mice.

Key Words: angiopoietin • eotaxin • antibody array • blood • inflammation




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