Search for: [Abstract = "Graft\-versus\-host disease \(GvHD\) is the major complication of allogeneic hematopoietic stem cell transplantation. Standard immunosuppressive regimen used for its prevention and treatment is only partially effective and it is associated with considerable side effects. This justifies further research focused on pathophysiology of GvHD and aiming at development of new strategies to control the disease. Recent research has shown that the complement system which is the central element of innate immunity also regulates adoptive immune response and tissue regeneration. Therefore, participation of complement in development of GvHD seems probable. This hypothesis is supported by involvement of complement in organ graft rejection. Activation of complement has been detected during GvHD in animal models and it has been suggested that it may participate in tissue injury observed in the course of the disease. However, there is lack of published data allowing to estimate the significance of complement for pathophysiology of GvHD. The aim of the study was to evaluate the role of complement in pathogenesis of GvHD employing C3 complement factor knock\-out animals. Within 14 experiments 119 C57BL\/6 C3 knock\-out \(C3\-\/\-\) mice and 104 C57BL\/6 wild\-type \(C3\+\/\+\) animals were transplanted with allogeneic bone marrow cells and splenocytes isolated from MHC mismatched C3H.He mice. Sex mismatched transpla"]

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