Activation‐induced deaminase–deficient MRL/lpr mice secrete high levels of protective antibodies against lupus nephritis
Objective We previously generated MRL/lpr mice deficient in activation‐induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice have high levels of unmutated (germline) autoreactive IgM, yet they experienced an increase in survival and an improvement in lupus...
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| Vydané v: | Arthritis & Rheumatism Ročník 63; číslo 4; s. 1086 - 1096 |
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| Hlavní autori: | , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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01.04.2011
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| Abstract | Objective
We previously generated MRL/lpr mice deficient in activation‐induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice have high levels of unmutated (germline) autoreactive IgM, yet they experienced an increase in survival and an improvement in lupus nephritis that exceeded that of MRL/lpr mice lacking IgG. The purpose of the present study was to test the hypothesis that high levels of germline autoreactive IgM in these mice confer protection against lupus nephritis.
Methods
Autoreactive IgM antibodies of various specificities, including antibodies against double‐stranded DNA (dsDNA), from AID‐deficient MRL/lpr mice were given to asymptomatic MRL/lpr mice, and the levels of cytokines, proteinuria, immune complex deposition in the kidneys, and glomerulonephritis were examined. Novel AID‐deficient MRL/lpr mice that lack any antibodies were generated for comparison to AID‐deficient MRL/lpr mice that secrete only IgM.
Results
Treatment with IgM anti‐dsDNA resulted in a dramatic improvement in lupus nephritis. Other autoreactive IgM antibodies, such as antiphospholipid and anti‐Sm, did not alter the pathologic changes. Secretion of proinflammatory cytokines by macrophages and the levels of inflammatory cells and apoptotic debris in the kidneys were lower in mice receiving IgM anti‐dsDNA. Protective IgM derived from AID‐deficient MRL/lpr mice displayed a distinct B cell repertoire, with a bias toward members of the VH7183 family.
Conclusion
IgM anti‐dsDNA protected MRL/lpr mice from lupus nephritis, likely by stopping the inflammatory cascade leading to kidney damage. A distinct repertoire of VH usage in IgM anti‐dsDNA hybridomas from AID‐deficient mice suggests that there is enrichment of a dedicated B cell population that secretes unmutated protective IgM in these mice. |
|---|---|
| AbstractList | Objective We previously generated MRL/lpr mice deficient in activation-induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice have high levels of unmutated (germline) autoreactive IgM, yet they experienced an increase in survival and an improvement in lupus nephritis that exceeded that of MRL/lpr mice lacking IgG. The purpose of the present study was to test the hypothesis that high levels of germline autoreactive IgM in these mice confer protection against lupus nephritis. Methods Autoreactive IgM antibodies of various specificities, including antibodies against double-stranded DNA (dsDNA), from AID-deficient MRL/lpr mice were given to asymptomatic MRL/lpr mice, and the levels of cytokines, proteinuria, immune complex deposition in the kidneys, and glomerulonephritis were examined. Novel AID-deficient MRL/lpr mice that lack any antibodies were generated for comparison to AID-deficient MRL/lpr mice that secrete only IgM. Results Treatment with IgM anti-dsDNA resulted in a dramatic improvement in lupus nephritis. Other autoreactive IgM antibodies, such as antiphospholipid and anti-Sm, did not alter the pathologic changes. Secretion of proinflammatory cytokines by macrophages and the levels of inflammatory cells and apoptotic debris in the kidneys were lower in mice receiving IgM anti-dsDNA. Protective IgM derived from AID-deficient MRL/lpr mice displayed a distinct B cell repertoire, with a bias toward members of the VH7183 family. Conclusion IgM anti-dsDNA protected MRL/lpr mice from lupus nephritis, likely by stopping the inflammatory cascade leading to kidney damage. A distinct repertoire of VH usage in IgM anti-dsDNA hybridomas from AID-deficient mice suggests that there is enrichment of a dedicated B cell population that secretes unmutated protective IgM in these mice. [PUBLICATION ABSTRACT] Objective We previously generated MRL/lpr mice deficient in activation‐induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice have high levels of unmutated (germline) autoreactive IgM, yet they experienced an increase in survival and an improvement in lupus nephritis that exceeded that of MRL/lpr mice lacking IgG. The purpose of the present study was to test the hypothesis that high levels of germline autoreactive IgM in these mice confer protection against lupus nephritis. Methods Autoreactive IgM antibodies of various specificities, including antibodies against double‐stranded DNA (dsDNA), from AID‐deficient MRL/lpr mice were given to asymptomatic MRL/lpr mice, and the levels of cytokines, proteinuria, immune complex deposition in the kidneys, and glomerulonephritis were examined. Novel AID‐deficient MRL/lpr mice that lack any antibodies were generated for comparison to AID‐deficient MRL/lpr mice that secrete only IgM. Results Treatment with IgM anti‐dsDNA resulted in a dramatic improvement in lupus nephritis. Other autoreactive IgM antibodies, such as antiphospholipid and anti‐Sm, did not alter the pathologic changes. Secretion of proinflammatory cytokines by macrophages and the levels of inflammatory cells and apoptotic debris in the kidneys were lower in mice receiving IgM anti‐dsDNA. Protective IgM derived from AID‐deficient MRL/lpr mice displayed a distinct B cell repertoire, with a bias toward members of the VH7183 family. Conclusion IgM anti‐dsDNA protected MRL/lpr mice from lupus nephritis, likely by stopping the inflammatory cascade leading to kidney damage. A distinct repertoire of VH usage in IgM anti‐dsDNA hybridomas from AID‐deficient mice suggests that there is enrichment of a dedicated B cell population that secretes unmutated protective IgM in these mice. We previously generated MRL/lpr mice deficient in activation-induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice have high levels of unmutated (germline) autoreactive IgM, yet they experienced an increase in survival and an improvement in lupus nephritis that exceeded that of MRL/lpr mice lacking IgG. The purpose of the present study was to test the hypothesis that high levels of germline autoreactive IgM in these mice confer protection against lupus nephritis.OBJECTIVEWe previously generated MRL/lpr mice deficient in activation-induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice have high levels of unmutated (germline) autoreactive IgM, yet they experienced an increase in survival and an improvement in lupus nephritis that exceeded that of MRL/lpr mice lacking IgG. The purpose of the present study was to test the hypothesis that high levels of germline autoreactive IgM in these mice confer protection against lupus nephritis.Autoreactive IgM antibodies of various specificities, including antibodies against double-stranded DNA (dsDNA), from AID-deficient MRL/lpr mice were given to asymptomatic MRL/lpr mice, and the levels of cytokines, proteinuria, immune complex deposition in the kidneys, and glomerulonephritis were examined. Novel AID-deficient MRL/lpr mice that lack any antibodies were generated for comparison to AID-deficient MRL/lpr mice that secrete only IgM.METHODSAutoreactive IgM antibodies of various specificities, including antibodies against double-stranded DNA (dsDNA), from AID-deficient MRL/lpr mice were given to asymptomatic MRL/lpr mice, and the levels of cytokines, proteinuria, immune complex deposition in the kidneys, and glomerulonephritis were examined. Novel AID-deficient MRL/lpr mice that lack any antibodies were generated for comparison to AID-deficient MRL/lpr mice that secrete only IgM.Treatment with IgM anti-dsDNA resulted in a dramatic improvement in lupus nephritis. Other autoreactive IgM antibodies, such as antiphospholipid and anti-Sm, did not alter the pathologic changes. Secretion of proinflammatory cytokines by macrophages and the levels of inflammatory cells and apoptotic debris in the kidneys were lower in mice receiving IgM anti-dsDNA. Protective IgM derived from AID-deficient MRL/lpr mice displayed a distinct B cell repertoire, with a bias toward members of the V(H) 7183 family.RESULTSTreatment with IgM anti-dsDNA resulted in a dramatic improvement in lupus nephritis. Other autoreactive IgM antibodies, such as antiphospholipid and anti-Sm, did not alter the pathologic changes. Secretion of proinflammatory cytokines by macrophages and the levels of inflammatory cells and apoptotic debris in the kidneys were lower in mice receiving IgM anti-dsDNA. Protective IgM derived from AID-deficient MRL/lpr mice displayed a distinct B cell repertoire, with a bias toward members of the V(H) 7183 family.IgM anti-dsDNA protected MRL/lpr mice from lupus nephritis, likely by stopping the inflammatory cascade leading to kidney damage. A distinct repertoire of V(H) usage in IgM anti-dsDNA hybridomas from AID-deficient mice suggests that there is enrichment of a dedicated B cell population that secretes unmutated protective IgM in these mice.CONCLUSIONIgM anti-dsDNA protected MRL/lpr mice from lupus nephritis, likely by stopping the inflammatory cascade leading to kidney damage. A distinct repertoire of V(H) usage in IgM anti-dsDNA hybridomas from AID-deficient mice suggests that there is enrichment of a dedicated B cell population that secretes unmutated protective IgM in these mice. We previously generated MRL/lpr mice deficient in activation-induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice have high levels of unmutated (germline) autoreactive IgM, yet they experienced an increase in survival and an improvement in lupus nephritis that exceeded that of MRL/lpr mice lacking IgG. The purpose of the present study was to test the hypothesis that high levels of germline autoreactive IgM in these mice confer protection against lupus nephritis. Autoreactive IgM antibodies of various specificities, including antibodies against double-stranded DNA (dsDNA), from AID-deficient MRL/lpr mice were given to asymptomatic MRL/lpr mice, and the levels of cytokines, proteinuria, immune complex deposition in the kidneys, and glomerulonephritis were examined. Novel AID-deficient MRL/lpr mice that lack any antibodies were generated for comparison to AID-deficient MRL/lpr mice that secrete only IgM. Treatment with IgM anti-dsDNA resulted in a dramatic improvement in lupus nephritis. Other autoreactive IgM antibodies, such as antiphospholipid and anti-Sm, did not alter the pathologic changes. Secretion of proinflammatory cytokines by macrophages and the levels of inflammatory cells and apoptotic debris in the kidneys were lower in mice receiving IgM anti-dsDNA. Protective IgM derived from AID-deficient MRL/lpr mice displayed a distinct B cell repertoire, with a bias toward members of the V(H) 7183 family. IgM anti-dsDNA protected MRL/lpr mice from lupus nephritis, likely by stopping the inflammatory cascade leading to kidney damage. A distinct repertoire of V(H) usage in IgM anti-dsDNA hybridomas from AID-deficient mice suggests that there is enrichment of a dedicated B cell population that secretes unmutated protective IgM in these mice. |
| Author | Jiang, Chuancang Zhao, Ming‐Lang Diaz, Marilyn Scearce, Richard M. |
| AuthorAffiliation | 1 Laboratory of Molecular Genetics, D3-01, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, Research Triangle Park, NC, 27709 3 Duke Human Vaccine Institute, 2 Genome Court, MSRBII 4102B, DUMC 103020, Durham, NC 27710 |
| AuthorAffiliation_xml | – name: 3 Duke Human Vaccine Institute, 2 Genome Court, MSRBII 4102B, DUMC 103020, Durham, NC 27710 – name: 1 Laboratory of Molecular Genetics, D3-01, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, Research Triangle Park, NC, 27709 |
| Author_xml | – sequence: 1 givenname: Chuancang surname: Jiang fullname: Jiang, Chuancang – sequence: 2 givenname: Ming‐Lang surname: Zhao fullname: Zhao, Ming‐Lang – sequence: 3 givenname: Richard M. surname: Scearce fullname: Scearce, Richard M. – sequence: 4 givenname: Marilyn surname: Diaz fullname: Diaz, Marilyn email: diaz@niehs.nih.gov |
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| Keywords | Kidney disease Immunopathology Connective tissue disease Skin disease Urinary system disease Antibody Rodentia Rheumatology Autoimmune disease Activation Lupus nephritis Prevention Vertebrata Mammalia Mouse Animal Systemic disease |
| Language | English |
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| Notes | Drs. Jiang and Zhao contributed equally to this work. Drs. Jiang, Zhao, and Diaz have a pending patent application for the use of unmutated IgM antibodies in the treatment of lupus nephritis. ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 Both of these authors contributed equally to this work |
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We previously generated MRL/lpr mice deficient in activation‐induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation.... We previously generated MRL/lpr mice deficient in activation-induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation. These mice... Objective We previously generated MRL/lpr mice deficient in activation-induced deaminase (AID) that lack isotype switching and immunoglobulin hypermutation.... |
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| SubjectTerms | AICDA (Activation-Induced Cytidine Deaminase) Animals Antibodies - metabolism Apoptosis - drug effects Apoptosis - physiology B-Lymphocytes - immunology B-Lymphocytes - metabolism Biological and medical sciences Cytidine Deaminase - deficiency Cytidine Deaminase - genetics Cytidine Deaminase - metabolism Disease Models, Animal Diseases of the osteoarticular system DNA - immunology Hybridomas - immunology Hybridomas - metabolism Immunoglobulin M - metabolism Immunoglobulin M - pharmacology Kidney - immunology Kidney - pathology Kidneys Lupus Lupus Erythematosus, Systemic - complications Lupus Erythematosus, Systemic - immunology Lupus Erythematosus, Systemic - metabolism Lupus Nephritis - metabolism Lupus Nephritis - pathology Lupus Nephritis - prevention & control Medical research Medical sciences Mice Mice, Inbred C57BL Mice, Inbred MRL lpr Mice, Knockout Nephrology. Urinary tract diseases Proteinuria - metabolism Rodents Urinary system involvement in other diseases. Miscellaneous |
| Title | Activation‐induced deaminase–deficient MRL/lpr mice secrete high levels of protective antibodies against lupus nephritis |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fart.30230 https://www.ncbi.nlm.nih.gov/pubmed/21225690 https://www.proquest.com/docview/1517062948 https://www.proquest.com/docview/859757071 https://pubmed.ncbi.nlm.nih.gov/PMC3079514 |
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