Cgnz1 allele confers kidney resistance to damage preventing progression of immune complex–mediated acute lupus glomerulonephritis

Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) dep...

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Published inThe Journal of experimental medicine Vol. 210; no. 11; pp. 2387 - 2401
Main Authors Ge, Yan, Jiang, Chao, Sung, Sun-Sang J., Bagavant, Harini, Dai, Chao, Wang, Hongyang, Kannapell, Carol C., Cathro, Helen P., Gaskin, Felicia, Man Fu, Shu
Format Journal Article
LanguageEnglish
Published United States The Rockefeller University Press 21.10.2013
Subjects
Acute Disease
Alleles
Animals
Antigen-Antibody Complex - adverse effects
Autoantibodies - adverse effects
Capillaries - pathology
Capillaries - ultrastructure
Chromosomes, Mammalian - genetics
Dendritic Cells - metabolism
Dendritic Cells - pathology
Disease Progression
Disease Susceptibility
Endocytosis
Endothelial Cells - pathology
Endothelial Cells - ultrastructure
Female
Gene Expression Regulation
Humans
Immunity - immunology
Inflammation - immunology
Inflammation - pathology
Kidney - blood supply
Kidney - immunology
Kidney - pathology
Kidney - ultrastructure
Lupus Nephritis - immunology
Lupus Nephritis - pathology
Macrophages - metabolism
Macrophages - pathology
Mice
Mice, Inbred Strains
Proteins - metabolism
Proteinuria - metabolism
Proteinuria - pathology
Sheep
Vacuoles - pathology
Vacuoles - ultrastructure
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Abstract Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti–mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.
AbstractList Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti–mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.
Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti-mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti-mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.
The mechanisms regulating acute and chronic glomerulonephritis are dependent on different genetic mechanisms, where the Cgnz1 allele confers kidney protection in immune complex-mediated proliferative lupus nephritis.
The mechanisms regulating acute and chronic glomerulonephritis are dependent on different genetic mechanisms, where the Cgnz1 allele confers kidney protection in immune complex–mediated proliferative lupus nephritis. Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was generated by introgressing a C57L/J region where Cgnz1 is located to NZM2328. R27 female mice developed aGN mediated by immune complex (IC) deposition and complement activation without progression to cGN with severe proteinuria. End stage renal disease (ESRD) was not seen in R27 mice as old as 15 mo. Thus, aGN and cGN are under separate genetic control, and IC-mediated proliferative GN need not progress to cGN and ESRD. NZM2328 and R27 female mice have comparable immune and inflammatory parameters. In contrast to NZM2328, R27 mice were resistant to sheep anti–mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediated by autoimmunity and resistance to the development of cGN is mediated by end organ resistance to damage. Thus, autoimmunity should be considered distinct from end organ damage. The Cgnz1 region has been mapped to a 1.34 MB region with 45 genes. Nine candidate genes were identified. Clinical relevance of these observations is supported by case studies. Clinical implications and the significance to human lupus and other diseases are presented.
Author Gaskin, Felicia
Wang, Hongyang
Jiang, Chao
Bagavant, Harini
Dai, Chao
Man Fu, Shu
Cathro, Helen P.
Ge, Yan
Sung, Sun-Sang J.
Kannapell, Carol C.
AuthorAffiliation 1 Division of Rheumatology and Immunology and 2 Center of Immunity, Inflammation and Regenerative Medicine, Department of Medicine ; 3 Department of Microbiology, Immunology and Cancer Biology ; 4 Division of Nephrology, Department of Medicine ; 5 Department of Pharmacology ; 6 Department of Pathology ; and 7 Department of Psychiatry and Neurobehavioral Sciences, University of Virginia School of Medicine, Charlottesville, VA 22908
AuthorAffiliation_xml – name: 1 Division of Rheumatology and Immunology and 2 Center of Immunity, Inflammation and Regenerative Medicine, Department of Medicine ; 3 Department of Microbiology, Immunology and Cancer Biology ; 4 Division of Nephrology, Department of Medicine ; 5 Department of Pharmacology ; 6 Department of Pathology ; and 7 Department of Psychiatry and Neurobehavioral Sciences, University of Virginia School of Medicine, Charlottesville, VA 22908
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C. Jiang’s present address is Molecular Immunology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20814.
Y. Ge’s present address is Genetics Institute, University of Florida, Gainesville, FL 32610.
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Snippet Cgnz1 and Agnz1 on the distal region of mouse chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN). NZM2328.Lc1R27 (R27) was...
The mechanisms regulating acute and chronic glomerulonephritis are dependent on different genetic mechanisms, where the Cgnz1 allele confers kidney protection...
The mechanisms regulating acute and chronic glomerulonephritis are dependent on different genetic mechanisms, where the Cgnz1 allele confers kidney protection...
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StartPage 2387
SubjectTerms Acute Disease
Alleles
Animals
Antigen-Antibody Complex - adverse effects
Autoantibodies - adverse effects
Capillaries - pathology
Capillaries - ultrastructure
Chromosomes, Mammalian - genetics
Dendritic Cells - metabolism
Dendritic Cells - pathology
Disease Progression
Disease Susceptibility
Endocytosis
Endothelial Cells - pathology
Endothelial Cells - ultrastructure
Female
Gene Expression Regulation
Humans
Immunity - immunology
Inflammation - immunology
Inflammation - pathology
Kidney - blood supply
Kidney - immunology
Kidney - pathology
Kidney - ultrastructure
Lupus Nephritis - immunology
Lupus Nephritis - pathology
Macrophages - metabolism
Macrophages - pathology
Mice
Mice, Inbred Strains
Proteins - metabolism
Proteinuria - metabolism
Proteinuria - pathology
Sheep
Vacuoles - pathology
Vacuoles - ultrastructure
Title Cgnz1 allele confers kidney resistance to damage preventing progression of immune complex–mediated acute lupus glomerulonephritis
URI https://www.ncbi.nlm.nih.gov/pubmed/24101379
https://www.proquest.com/docview/1444392342
https://www.proquest.com/docview/1551640863
https://pubmed.ncbi.nlm.nih.gov/PMC3804943
Volume 210
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