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Integrin α2β1 deficiency does not affect contact hypersensitivity

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Abstract

Collagens in the extracellular matrix are thought to play an important role in regulating inflammatory responses by affecting cell adhesion and migration. The contact between collagens and cells is established mainly by α1β1, α2β1 and α11β1integrin receptors. Here, we analyzed the contact hypersensitivity (CHS) reaction in mice that were genetically deficient in the collagen receptor α2β1. Integrin α2β1 is widely expressed and has been suggested to play an important role in mediating inflammatory responses. CHS was induced by applying dinitrofluorobenzene to abdominal skin and challenging with the same reagent on ear skin. Macroscopically and histologically, ear swelling in α2β1-deficient mice did not differ from that in wild-type control mice. Immunohistological detection of infiltrated T lymphocytes, neutrophils and mast cells in inflamed ear skin revealed similar numbers in controls and integrin α2β1-deficient animals. Our results suggest that the adhesive functions of integrin α2β1 are dispensable for the CHS response; they may be compensated for by the collagen receptor α1β1 or other collagen receptors.

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Acknowledgments

We thank Dr. Ingo Haase for stimulating discussion and Nicole Brüggenolte and Silke Kummer for excellent technical assistance. This study was supported by the Deutsche Forschungsgemeinschaft through the SFB 589 at the University of Cologne.

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Correspondence to Beate Eckes.

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Zweers, M.C., Siewe, L., Wickenhauser, C. et al. Integrin α2β1 deficiency does not affect contact hypersensitivity. Arch Dermatol Res 298, 201–205 (2006). https://doi.org/10.1007/s00403-006-0688-7

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  • DOI: https://doi.org/10.1007/s00403-006-0688-7

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