| Deficiency in activation-induced cytidine deaminase promotes systemic autoimmunity in lpr mice on a C57BL/6 background. | |
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MedLine Citation:
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PMID: 19922498 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Activation-induced deaminase (AID) is a prerequisite for immunoglobulin (Ig) class-switch recombination and somatic hypermutation, which is critical for antibody affinity maturation. IgM and IgG autoantibodies are characteristic of the systemic autoimmune disorders such as lupus. However, the relative contributions of hypermutated high-affinity IgG antibodies and germline-encoded IgM antibodies to systemic autoimmunity are not defined fully. The role of AID in autoimmunity is unclear. The current study used AID-deficient mice to investigate the role of AID in the development and pathogenesis of murine lupus. C57BL/6 mice deficient in both Fas and AID were generated. Compared to their AID-competent littermates, AID(-/-) lymphoproliferative (lpr) mice produced significantly elevated levels of IgM autoreactive antibodies with enhanced germinal centre (GC) response, developed more advanced splenomegaly and exhibited more severe glomerulonephritis. Thus, AID may play an important role in the negative regulation of systemic autoimmune manifestations in murine lupus. The results also indicate that hypermutated high-affinity IgG antibodies are not necessary for the development of autoimmune syndrome in lpr mice on a C57BL/6 background. |
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Authors:
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L Chen; L Guo; J Tian; B Zheng; S Han |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-11-18 |
Journal Detail:
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Title: Clinical and experimental immunology Volume: 159 ISSN: 1365-2249 ISO Abbreviation: Clin. Exp. Immunol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-18 Completed Date: 2010-02-03 Revised Date: 2011-07-22 |
Medline Journal Info:
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Nlm Unique ID: 0057202 Medline TA: Clin Exp Immunol Country: England |
Other Details:
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Languages: eng Pagination: 169-75 Citation Subset: IM |
Affiliation:
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Department of Immunology, Baylor College of Medicine, Houston, TX, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, CD3 / metabolism Autoantibodies / blood Autoimmune Diseases / enzymology*, genetics, immunology Crosses, Genetic Cytidine Deaminase / deficiency*, genetics Female Flow Cytometry Germinal Center / immunology, metabolism, pathology Glomerulonephritis / enzymology, genetics, pathology Immunoglobulin M / blood Male Mice Mice, Inbred C57BL Mice, Inbred MRL lpr Mice, Knockout Splenomegaly / enzymology, genetics, pathology T-Lymphocytes / immunology, metabolism, pathology Urinalysis |
| Grant Support | |
ID/Acronym/Agency:
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AI051532/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD3; 0/Autoantibodies; 0/Immunoglobulin M; EC 3.5.4.-/AICDA (activation-induced cytidine deaminase); EC 3.5.4.5/Cytidine Deaminase |
| Comments/Corrections | |
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