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PMID:9927509
| Citation |
Vora, KA, Tumas-Brundage, KM, Lentz, VM, Cranston, A, Fishel, R and Manser, T (1999) Severe attenuation of the B cell immune response in Msh2-deficient mice. J. Exp. Med. 189:471-82 |
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| Abstract |
Recently, results obtained from mice with targeted inactivations of postreplication DNA mismatch repair (MMR) genes have been interpreted to demonstrate a direct role for MMR in antibody variable (V) gene hypermutation. Here we show that mice that do not express the MMR factor Msh2 have wide-ranging defects in antigen-driven B cell responses. These include lack of progression of the germinal center (GC) reaction associated with increased intra-GC apoptosis, severely diminished antigen-specific immunoglobulin G responses, and near absence of anamnestic responses. Mice heterozygous for the Msh2 deficiency display an "intermediate" phenotype in these regards, suggesting that normal levels of Msh2 expression are critical for the B cell response. Interpretation of the impact of an MMR deficiency on the mechanism of V gene somatic hypermutation could be easily confounded by these perturbations. |
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| Keywords |
Animals; Antibodies/blood; Apoptosis; B-Lymphocytes/immunology; Bone Marrow Cells/immunology; DNA Repair; DNA-Binding Proteins; Germinal Center/immunology; Heterozygote; Homozygote; Immune System/abnormalities; Immunoglobulin Class Switching; Immunoglobulin Isotypes; Lymphocyte Activation; Mice; Mice, Mutant Strains; MutS Homolog 2 Protein; Proto-Oncogene Proteins/deficiency; Proto-Oncogene Proteins/genetics; Spleen/immunology; T-Lymphocytes/immunology |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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