NDLI: Apurinic/apyrimidinic endonuclease 2 regulates the expansion of germinal centers by protecting against activation-induced cytidine deaminase-independent DNA damage in B cells.

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Apurinic/apyrimidinic endonuclease 2 regulates the expansion of germinal centers by protecting against activation-induced cytidine deaminase-independent DNA damage in B cells.

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Apurinic/apyrimidinic endonuclease 2 regulates the expansion of germinal centers by protecting against activation-induced cytidine deaminase-independent DNA damage in B cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Woodland, Robert T. Esa, Nada Linehan, Erin K. Nakabeppu, Yusaku Tsuchimoto, Daisuke Guikema, Jeroen E. J. Schrader, Carol E.
Description	Author Affiliation: Guikema JE ( Department of Molecular and Physiological Systems, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, MA 01655); Linehan EK ( Department of Molecular and Physiological Systems, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, MA 01655); Esa N ( Department of Molecular and Physiological Systems, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, MA 01655); Tsuchimoto D ( Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan.); Nakabeppu Y ( Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan.); Woodland RT ( Department of Molecular and Physiological Systems, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, MA 01655); Schrader CE ( Department of Molecular and Physiological Systems, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, MA 01655)
Abstract	Activation-induced cytidine deaminase (AID) initiates a process generating DNA mutations and breaks in germinal center (GC) B cells that are necessary for somatic hypermutation and class-switch recombination. GC B cells can 'tolerate' DNA damage while rapidly proliferating because of partial suppression of the DNA damage response by BCL6. In this study, we develop a model to study the response of mouse GC B cells to endogenous DNA damage. We show that the base excision repair protein apurinic/apyrimidinic endonuclease (APE) 2 protects activated B cells from oxidative damage in vitro. APE2-deficient mice have smaller GCs and reduced Ab responses compared with wild-type mice. DNA double-strand breaks are increased in the rapidly dividing GC centroblasts of APE2-deficient mice, which activate a p53-independent cell cycle checkpoint and a p53-dependent apoptotic response. Proliferative and/or oxidative damage and AID-dependent damage are additive stresses that correlate inversely with GC size in wild-type, AID-, and APE2-deficient mice. Excessive double-strand breaks lead to decreased expression of BCL6, which would enable DNA repair pathways but limit GC cell numbers. These results describe a nonredundant role for APE2 in the protection of GC cells from AID-independent damage, and although GC cells uniquely tolerate DNA damage, we find that the DNA damage response can still regulate GC size through pathways that involve p53 and BCL6.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400002
Journal	The Journal of Immunology
Issue Number	2
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	B-lymphocytes Immunology Cytidine Deaminase Dna Damage Endonucleases Germinal Center Animals Apoptosis Genetics Metabolism Cell Cycle Cell Proliferation Cells, Cultured Deficiency Dna Breaks, Double-stranded Dna-binding Proteins Flow Cytometry Immunoglobulin Class Switching Lymphocyte Activation Mice Mice, Inbred C57bl Mice, Inbred Strains Mice, Knockout Oxidative Stress Proto-oncogene Proteins C-bcl-6 Reactive Oxygen Species Somatic Hypermutation, Immunoglobulin Tumor Suppressor Protein P53 Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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