Supportive evidence of the importance of the contribution of the activated complement system includes the decrease in cure rates of PDT-treated tumours following blockage of complement activation by the inhibitor FUT-175 (Korbelik, 2006), or specific inactivation of complement anaphylatoxins C3a and C5a (Cecic et al, 2005).
Multiple studies have stressed the importance of the contribution of activated complement to the pathology of reperfusion injury after tissue ischemia.
The 'Four Core Genotypes' mouse model has been used to dissect the contribution of sex-chromosome complement and the organisational and activational effects of sex-specific hormones [ 6], revealing that both hormones and chromosomal complement exert independent and divergent effects over metabolic and behavioural phenotypes [ 7, 8].
In this study, we report for the first time the important contribution of the lectin pathway of complement activation to brain tissue fate after acute stroke, both in mice and humans.
Thus, genetic and gonadal sex are dissociated in the FCG mice, and the contribution of sex chromosome complement can be investigated independently (reviewed in [ 75]).
Another mouse model that is useful for studying the contribution of sex chromosome complement to sex differences is the steroidogenic factor 1 (SF-1) KO mouse.
Data from studies of the effect of those antibodies in murine models established a contribution of complement activation to the placental inflammation, TNF production, neutrophil accumulation and fetal death that mimics the events that sometimes occur in lupus patients with antiphospholipid antibodies [ 51, 52].
Using the FCG mice, investigators can independently assess the contribution of sex chromosome complement, developmental hormone exposure, and adult circulating hormones to various observed sex differences.
To evaluate the contribution of complement 3 (C3) or C3a toward these abnormalities in SHR, we examined effects of a C3a receptor inhibitor on proliferation, phenotype, and Ang II-production in VSMCs from SHR and Wistar Kyoto (WKY) rats.
To establish the contribution of complement-mediated injury to the allograft microcirculation, we transplanted C3-deficient and C3-inhibited recipients.
