| First Author | Vora KA | Year | 1999 |
| Journal | J Exp Med | Volume | 189 |
| Issue | 3 | Pages | 471-82 |
| PubMed ID | 9927509 | Mgi Jnum | J:52568 |
| Mgi Id | MGI:1329767 | Doi | 10.1084/jem.189.3.471 |
| Citation | Vora KA, et al. (1999) Severe attenuation of the B cell immune response in Msh2-deficient mice. J Exp Med 189(3):471-82 |
| abstractText | 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. |
