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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.<\/jats:p>","DOI":"10.4049\/jimmunol.169.7.3819","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T19:18:01Z","timestamp":1398107881000},"page":"3819-3824","source":"Crossref","is-referenced-by-count":13,"title":["<i>Bcl-2<\/i>\n                    Rescues the Germinal Center Response But Does Not Alter the V Gene Somatic Hypermutation Spectrum in MSH2-Deficient Mice"],"prefix":"10.1093","volume":"169","author":[{"given":"Boris","family":"Alabyev","sequence":"first","affiliation":[{"name":"Kimmel Cancer Center and Department of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University Philadelphia , PA 19107"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tim","family":"Manser","sequence":"additional","affiliation":[{"name":"Kimmel Cancer Center and Department of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University Philadelphia , PA 19107"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2002,10,1]]},"reference":[{"key":"2026020209245966400_R1","first-page":"141","volume-title":"Immunol. 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