| First Author | Alabyev B | Year | 2002 |
| Journal | J Immunol | Volume | 169 |
| Issue | 7 | Pages | 3819-24 |
| PubMed ID | 12244177 | Mgi Jnum | J:120202 |
| Mgi Id | MGI:3704040 | Doi | 10.4049/jimmunol.169.7.3819 |
| Citation | Alabyev B, et al. (2002) Bcl-2 rescues the germinal center response but does not alter the V gene somatic hypermutation spectrum in MSH2-deficient mice. J Immunol 169(7):3819-24 |
| abstractText | 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. |
