Zweers Manon C, Siewe Lisa, Wickenhauser Claudia, Krieg Thomas, Roers Axel, Eckes Beate
Department of Dermatology, University of Cologne, Kerpener Str. 62, 50937 Cologne, Germany.
Arch Dermatol Res. 2006 Sep;298(4):201-5. doi: 10.1007/s00403-006-0688-7. Epub 2006 Aug 5.
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 alpha1beta1, alpha2beta1 and alpha11beta1integrin receptors. Here, we analyzed the contact hypersensitivity (CHS) reaction in mice that were genetically deficient in the collagen receptor alpha2beta1. Integrin alpha2beta1 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 alpha2beta1-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 alpha2beta1-deficient animals. Our results suggest that the adhesive functions of integrin alpha2beta1 are dispensable for the CHS response; they may be compensated for by the collagen receptor alpha1beta1 or other collagen receptors.
细胞外基质中的胶原蛋白被认为通过影响细胞黏附和迁移在调节炎症反应中发挥重要作用。胶原蛋白与细胞之间的接触主要通过α1β1、α2β1和α11β1整合素受体建立。在此，我们分析了胶原蛋白受体α2β1基因缺陷小鼠的接触性超敏反应（CHS）。整合素α2β1广泛表达，并且已被认为在介导炎症反应中发挥重要作用。通过将二硝基氟苯涂抹于腹部皮肤并在耳部皮肤用相同试剂激发来诱导CHS。在宏观和组织学上，α2β1缺陷小鼠的耳部肿胀与野生型对照小鼠并无差异。对发炎耳部皮肤中浸润的T淋巴细胞、中性粒细胞和肥大细胞进行免疫组织学检测发现，对照动物和整合素α2β1缺陷动物中的细胞数量相似。我们的结果表明，整合素α2β1的黏附功能对于CHS反应并非必需；它们可能由胶原蛋白受体α1β1或其他胶原蛋白受体代偿。
