Knock out Mice Models for Immunodeficiency Diseases
The impressive progress in transgenic techniques in mice within the past ten years has opened up valuable new experimental approaches to immunologists. For many research purposes it is of great interest to eliminate a specific gene or at least to prevent the normal function of its product. A well known example are transgenic mice with rearranged antigen receptor genes preventing the diversification of whole lymphocyte subsets via allelic exclusion. Such antigen receptor transgenic mice have been successfully used to study T- and B-cell development (Storb 1987, Goodnow et al 1988, von Boehmer 1990). The direct modification of genes in the mouse germline could be achieved in the past only by insertional mutagenesis using transgenes or retroviruses, and chemical- or radiation-induced mutagenesis (for review see Jaenisch 1988). The limitation of these strategies is that the gene to be mutated and the exact nature of the mutation cannot be predetermined. The accuracy by which mutations can be introduced into the mouse genome has been greatly improved with the development of gene targeting techniques within the last four years allowing the modification of a particular gene in a predetermined manner (for review see Capecchi 1989, Gridley et al 1991, Bradley et al 1992).
KeywordsOsteogenesis Imperfecta Severe Combine Immunodeficiency Lymphocytic Choriomeningitis Allelic Exclusion Adenosine Deaminase Deficiency
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