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Protective Responses of Endothelial Cells

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Genes and Resistance to Disease

Summary

Endothelial cells (EC) as they normally exist in their quiescent state perform critical functions in maintaining blood flow and avoiding thrombosis. Various proinflammatory stimuli can induce EC to be activated, which results in recruitment, trans-endothelial migration and activation of circulating leukocytes, procoagulation, platelet aggregation, and other responses associated with inflammation. In the case of an organ that is transplanted, these reactions associated with EC activation accompany the rejection of such organ. We suggested, several years ago, that EC activation is the underlying basis of rejection of organ xenografts, i.e., grafts such as a heart or kidney transplanted across different species. While antibodies and complement in the recipient are clearly implicated in EC activation and xenograft rejection, investigators in the 1980s showed that, under certain circumstances, grafts can survive indefinitely despite the presence of antigraft antibodies and complement. We referred to the survival of an organ in the presence of anti-organ antibodies and complement as “accommodation.” One possible mechanism that we proposed to explain accommodation of these grafts was that, under certain circumstances the EC in the graft up-regulate the expression of “protective genes” that would prevent those reactions associated with EC activation that presumably lead to rejection. We have since found that such protective genes do exist and that they can play such a role.

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Soares, M.P. et al. (2000). Protective Responses of Endothelial Cells. In: Boulyjenkov, V., Berg, K., Christen, Y. (eds) Genes and Resistance to Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56947-0_9

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  • DOI: https://doi.org/10.1007/978-3-642-56947-0_9

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