CD18 in Monogenic and Polygenic Inflammatory Processes of the Skin.
The beta(2) integrin family (CD11/ CD18) of leukocyte adhesion molecules plays a key role in inflammation. Absence of the common beta chain ( CD18) leads to leukocyte adhesion deficiency-1 (LAD1) in humans. We here summarize data of two genetically defined mice models of beta(2) integrin deficiency, one with a CD18 null mutation ( CD18(-/-)), and the other one with a hypomorphic CD18 mutation (CD18(hypo)). Firstly, we focus on the underlying mechanism of a severely impaired wound healing in CD18(-/-) mice, outlining a scenario in which a defective extravasation and phagocytosis of CD18(-/-) neutrophils results in delayed myofibroblast-dependent wound contraction owing to a deficient transforming growth factor-beta(1) release. Based on this, we have identified a potential therapy that fully rescued the impaired wound healing in CD18(-/-) mice. Secondly, we expand on a CD18(hypo) PL/J mouse model closely resembling human psoriasis. Apart from common clinical and pathophysiological features, this psoriasiform dermatitis also depends on the presence of activated CD4(+)T cells. We here recapitulate the influence of a reduced CD18 gene expression on T-cell function, also with regard to CD18 gene-dose effects, and its contribution to the pathogenesis of this disease. Taken together, these unique features make this model a valuable tool for investigations into the pathogenesis of human psoriasis - including its polygenic base - and future preclinical studies.Journal of Investigative Dermatology Symposium Proceedings (2006) 11, 7-15. doi:10.1038/sj.jidsymp.5650006.[1]References
- CD18 in Monogenic and Polygenic Inflammatory Processes of the Skin. Peters, T., Sindrilaru, A., Wang, H., Oreshkova, T., Renkl, A.C., Kess, D., Scharffetter-Kochanek, K. J. Invest. Dermatol. (2006) [Pubmed]
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