Document Detail


Impaired lymphocyte development and antibody class switching and increased malignancy in a murine model of DNA ligase IV syndrome.
MedLine Citation:
PMID:  19451691     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypomorphic mutations in DNA ligase IV (LIG4) cause a human syndrome of immunodeficiency, radiosensitivity, and growth retardation due to defective DNA repair by the nonhomologous end-joining (NHEJ) pathway. Lig4-null mice are embryonic lethal, and better mouse models are needed to study human LigIV syndrome. We recently identified a viable mouse strain with a Y288C hypomorphic mutation in the Lig4 gene. Lig4Y288C mice exhibit a greater than 10-fold reduction of LigIV activity in vivo and recapitulate the immunodeficiency and growth retardation seen in human patients. Here, we have demonstrated that the Lig4Y288C mutation leads to multiple defects in lymphocyte development and function, including impaired V(D)J recombination, peripheral lymphocyte survival and proliferation, and B cell class switch recombination. We also highlight a high incidence of thymic tumors in the Lig4Y288C mice, suggesting that wild-type LigIV protects against malignant transformation. These findings provide explanations for the complex lymphoid phenotype of human LigIV syndrome.
Authors:
Anastasia Nijnik; Sara Dawson; Tanya L Crockford; Lisa Woodbine; Supawan Visetnoi; Sophia Bennett; Margaret Jones; Gareth D Turner; Penelope A Jeggo; Christopher C Goodnow; Richard J Cornall
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-18
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  119     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-06-02     Completed Date:  2009-07-24     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1696-705     Citation Subset:  AIM; IM    
Affiliation:
Henry Wellcome Building of Molecular Physiology, Oxford University, Oxford, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibody Formation / immunology
Cell Differentiation / immunology*
Cell Survival
DNA Ligases / deficiency,  genetics,  metabolism*
Disease Models, Animal
Immunoglobulin Class Switching / immunology*
Immunoglobulin Isotypes / immunology*
Lymphocytes / cytology,  enzymology*,  immunology*
Mice
Mice, Inbred C57BL
Mice, Knockout
Mutation / genetics
Syndrome
Thymus Neoplasms / enzymology*,  genetics,  immunology,  pathology
Grant Support
ID/Acronym/Agency:
//Department of Health; //Medical Research Council; //Wellcome Trust
Chemical
Reg. No./Substance:
0/Immunoglobulin Isotypes; EC 6.5.1.-/DNA Ligases
Comments/Corrections

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