Background: The complement cascade is increasingly implicated in development of a variety of diseases with\nstrong immune contributions such as Alzheimerâ??s disease and Systemic Lupus Erythematosus. Mouse models have\nbeen used to determine function of central components of the complement cascade such as C1q and C3.\nHowever, species differences in their gene structures mean that mice do not adequately replicate human\ncomplement regulators, including CR1 and CR2. Genetic variation in CR1 and CR2 have been implicated in\nmodifying disease states but the mechanisms are not known.\nResults: To decipher the roles of human CR1 and CR2 in health and disease, we engineered C57BL/6J (B6) mice to\nreplace endogenous murine Cr2 with human complement receptors, CR1 and CR2 (B6.CR2CR1). CR1 has an array of\nallotypes in human populations and using traditional recombination methods (Flp-frt and Cre-loxP) two of the most\ncommon alleles.............................
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