HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Alabyev, B. Articles by Manser, T. Search for Related Content PubMed PubMed Citation Articles by Alabyev, B. Articles by Manser, T. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene

Bcl-2 Rescues the Germinal Center Response But Does Not Alter the V Gene Somatic Hypermutation Spectrum in MSH2-Deficient Mice¹

Kimmel Cancer Center and Department of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University Philadelphia, PA 19107

Ab V genes in mice deficient for the postreplication mismatch repair factor MutS homolog (MSH2) have been reported to display an abnormal bias for hypermutations at G and C nucleotides and hotspots. We previously showed that the germinal center (GC) response is severely attenuated in MSH2-deficient mice. This suggested that premature death of GC B cells might preclude multiple rounds of hypermutation necessary to generate a normal spectrum of base changes. To test this hypothesis, we created MSH2-deficient mice in which Bcl-2 expression was driven in B cells from a transgene. In such mice, the elevated levels of intra-GC apoptosis and untimely GC dissolution characteristic of MSH2-deficient mice are suppressed. However, the spectrum of hypermutation is unchanged. These data indicate that the effects of MSH2 deficiency on GC B cell viability and the hypermutation process are distinct.

This article has been cited by other articles:

				Z. S. M. Rahman, B. Alabyev, and T. Manser Fc{gamma}RIIB Regulates Autoreactive Primary Antibody-Forming Cell, but Not Germinal Center B Cell, Activity J. Immunol., January 15, 2007; 178(2): 897 - 907. [Abstract] [Full Text] [PDF]

				Z. S. M. Rahman and T. Manser Failed Up-Regulation of the Inhibitory IgG Fc Receptor Fc{gamma}RIIB on Germinal Center B Cells in Autoimmune-Prone Mice Is Not Associated with Deletion Polymorphisms in the Promoter Region of the Fc{gamma}RIIB Gene J. Immunol., August 1, 2005; 175(3): 1440 - 1449. [Abstract] [Full Text] [PDF]

				Z. S. M. Rahman and T. Manser B Cells Expressing Bcl-2 and a Signaling-Impaired BAFF-Specific Receptor Fail to Mature and Are Deficient in the Formation of Lymphoid Follicles and Germinal Centers J. Immunol., November 15, 2004; 173(10): 6179 - 6188. [Abstract] [Full Text] [PDF]

				M. Cascalho Advantages and Disadvantages of Cytidine Deamination J. Immunol., June 1, 2004; 172(11): 6513 - 6518. [Abstract] [Full Text] [PDF]

				Z. SM. Rahman, S. P. Rao, S. L. Kalled, and T. Manser Normal Induction but Attenuated Progression of Germinal Center Responses in BAFF and BAFF-R Signaling-Deficient Mice J. Exp. Med., October 20, 2003; 198(8): 1157 - 1169. [Abstract] [Full Text] [PDF]

				A. Martin, Z. Li, D. P. Lin, P. D. Bardwell, M. D. Iglesias-Ussel, W. Edelmann, and M. D. Scharff Msh2 ATPase Activity Is Essential for Somatic Hypermutation at A-T Basepairs and for Efficient Class Switch Recombination J. Exp. Med., October 20, 2003; 198(8): 1171 - 1178. [Abstract] [Full Text] [PDF]

				P. D. Bardwell, A. Martin, E. Wong, Z. Li, W. Edelmann, and M. D. Scharff Cutting Edge: The G-U Mismatch Glycosylase Methyl-CpG Binding Domain 4 Is Dispensable for Somatic Hypermutation and Class Switch Recombination J. Immunol., February 15, 2003; 170(4): 1620 - 1624. [Abstract] [Full Text] [PDF]