Phenotypes of complement knockouts.
Although complete and partial complement deficiencies are well described in humans and several spontaneous animal models, many questions have remained regarding the exact role that these deficiency states play in the observed clinical manifestations. Likewise, many important mechanistic questions cannot be addressed using patients or spontaneously arising animal models of deficiency states. To provide additional insights and create readily manipulable experimental systems, over the last 5 years mice have been created by several groups in which specifically targeted insertional mutagenesis has resulted in complete deficiencies of complement activation proteins, receptors or regulatory proteins. Many surprising findings have already been made using mice derived from these strategies, and clinically relevant studies have begun to provide great insights into human deficiency states. This review includes an overview of these complement deficient mice and highlights some of the important findings that have resulted from their creation. A discussion of future experimental directions thought to be important by this author then follows and concludes the review.
Holers
V M
VM
Division of Rheumatology, Box B-115, University of Colorado Health Sciences Center, Denver 80262, USA. michael.holers@uchsc.edu
D000818:Animals; D018958:CD55 Antigens / Q000235:genetics / Q000502:physiology; D003167:Complement Activation / Q000235:genetics; D011415:Complement Factor B / Q000172:deficiency / Q000235:genetics; D003165:Complement System Proteins / Q000172:deficiency* / Q000235:genetics; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D010641:Phenotype; D011951:Receptors, Complement / Q000172:deficiency / Q000235:genetics; D000683:Serum Amyloid P-Component / Q000172:deficiency / Q000235:genetics
D018958:CD55 Antigens; D011951:Receptors, Complement; D000683:Serum Amyloid P-Component; D003165:Complement System Proteins; D011415:Complement Factor B