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CD59a is the primary regulator of membrane attack complex assembly in the mouse

Baalasubramanian, Sivasankar, Harris, Claire Louise, Donev, Rossen Mintchev, Mizuno, Masashi, Omidvar, Nader, Song, Wen-Chao and Morgan, Bryan Paul ORCID: 2004. CD59a is the primary regulator of membrane attack complex assembly in the mouse. Journal of Immunology 173 , pp. 3684-3692.

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Gene-deleted mice have provided a potent tool in efforts to understand the roles of complement and complement-regulating proteins in vivo. In particular, mice deficient in the membrane regulators complement receptor 1-related gene/protein y, decay-accelerating factor, or CD59 have demonstrated homeostatic relevance and backcrossing between the strains has revealed cooperativity in regulation. In mouse, genes encoding decay-accelerating factor and CD59 have been duplicated and show differential expression in tissues, complicating interpretation and extrapolation of findings to man. The first described form of CD59, CD59a, is broadly distributed and deletion of the cd59a gene causes a mild hemolytic phenotype with increased susceptibility in complement-mediated disease models. The distribution of the second form, CD59b, was originally described as testis specific, but later by some as widespread. Deletion of the cd59b gene caused a severe hemolytic and thrombotic phenotype. To apply data from these mouse models to man it is essential to know the relative distribution and functional roles of these two forms of CD59. We have generated new specific reagents and used them in sensitive quantitative analyses to comprehensively characterize expression of mRNA and protein and functional roles of CD59a and CD59b in wild-type (wt) and CD59a-negative mice. cd59b mRNA was detected only in testis and, at very low levels, in bone marrow. CD59b protein was present on mature spermatozoa and precursors and, in trace amounts, erythrocytes. Erythrocyte CD59b did not inhibit complement lysis except when CD59a was absent or blocked. These data confirm that CD59a is the primary regulator of complement membrane attack in mouse.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: Q Science > QH Natural history > QH426 Genetics
R Medicine > R Medicine (General)
Uncontrolled Keywords: Animals Antibodies, Monoclonal/biosynthesis Antigens, CD59/biosynthesis Antigens, CD59/genetics Antigens, CD59/immunology Antigens, CD59/physiology* Complement Activation/immunology Complement Membrane Attack Complex/metabolism* Erythrocytes/immunology Erythrocytes/metabolism Hemolysis/immunology Male Mice Mice, Inbred C57BL Mice, Knockout Organ Specificity/immunology Polymerase Chain Reaction Precipitin Tests Protein Isoforms/biosynthesis Protein Isoforms/genetics Protein Isoforms/immunology Protein Isoforms/physiology Protein Processing, Post-Translational/immunology* RNA, Messenger/biosynthesis Testis/immunology Testis/metabolism
ISSN: 1048-3233
Last Modified: 17 Oct 2022 08:27

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