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Genetically Determined Murine Models of Immunodeficiency

Genetically Determined Murine Models of Immunodeficiency Numerous investigations of the mammalian immune system in normal and pathologic states have been facilitated by the study of genetically determined immunologic dysfunctions in experimental animals. Heritable immunologic defects in mice have been studied extensively as models for immunodeficiency and autoimmune diseases of humans. This article focuses on mutations of the mouse that cause impairments in thc devel­ opment or regulation of the immune system. Since spontaneous murine autoimmune disease has been the subject of numerous reviews ( 1-4), genetically determined murine immunodeficiency disorders are stressed. Investigations into basic mechanisms underlying the function of the mammalian immune system have benefited greatly by the development of inbred strains. However, the complex developmental and functional relationships within the immune system have made it difficult to elucidate those mechanisms that underlie genetically determined immunologic dys­ function in humans. Early experiments using heritable defects in mice to learn about normal immunologic processes focused on NZB mice and the (NZB x NZW)F] hybrid. These mice have functional defects in their T cells, B cells, and macrophages which yield a wide spectrum of immu­ nologic abnormalities, including polyclonal immunoglobulin (Ig) pro­ duction, autoantibodies, and immune complex disease (1-4). Unfor­ tunately,the genetic bases of immunologic http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Immunology Annual Reviews

Genetically Determined Murine Models of Immunodeficiency

Annual Review of Immunology , Volume 5 (1) – Apr 1, 1987

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Publisher
Annual Reviews
Copyright
Copyright 1987 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0732-0582
eISSN
1545-3278
DOI
10.1146/annurev.iy.05.040187.002055
pmid
3297105
Publisher site
See Article on Publisher Site

Abstract

Numerous investigations of the mammalian immune system in normal and pathologic states have been facilitated by the study of genetically determined immunologic dysfunctions in experimental animals. Heritable immunologic defects in mice have been studied extensively as models for immunodeficiency and autoimmune diseases of humans. This article focuses on mutations of the mouse that cause impairments in thc devel­ opment or regulation of the immune system. Since spontaneous murine autoimmune disease has been the subject of numerous reviews ( 1-4), genetically determined murine immunodeficiency disorders are stressed. Investigations into basic mechanisms underlying the function of the mammalian immune system have benefited greatly by the development of inbred strains. However, the complex developmental and functional relationships within the immune system have made it difficult to elucidate those mechanisms that underlie genetically determined immunologic dys­ function in humans. Early experiments using heritable defects in mice to learn about normal immunologic processes focused on NZB mice and the (NZB x NZW)F] hybrid. These mice have functional defects in their T cells, B cells, and macrophages which yield a wide spectrum of immu­ nologic abnormalities, including polyclonal immunoglobulin (Ig) pro­ duction, autoantibodies, and immune complex disease (1-4). Unfor­ tunately,the genetic bases of immunologic

Journal

Annual Review of ImmunologyAnnual Reviews

Published: Apr 1, 1987

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