PMID:9697842

Citation	Frey, S, Bertocci, B, Delbos, F, Quint, L, Weill, JC and Reynaud, CA (1998) Mismatch repair deficiency interferes with the accumulation of mutations in chronically stimulated B cells and not with the hypermutation process. Immunity 9:127-34
Abstract	Primary responses to the hapten phenyloxazolone and chronic responses to environmental antigens occurring in Peyer's patches were analyzed in two different mismatch repair-deficient backgrounds. Paradoxically, whereas primary responses were found normal in MSH2- and only slightly diminished in PMS2-deficient mice, mutations in Peyer's patch B cells from both k.o. animals were reduced three times, the subset of Peyer's patch B cells with highly mutated sequences being specifically missing in the mismatch repair-deficient context. Strikingly, germinal center B cells from Peyer's patches of k.o. animals showed microsatellite instability at an unprecedented level. We thus propose that the amount of DNA damages generated prevents these cells from recycling in germinal centers and that mismatch repair deficiency is only the indirect cause of the lower mutation incidence observed.
Links	PubMed
Keywords	Adenosine Triphosphatases; Animals; B-Lymphocytes; Base Sequence; Cell Line; DNA Repair; DNA Repair Enzymes; DNA-Binding Proteins; Genes, Immunoglobulin; Germinal Center; Haptens/administration & dosage; Mice; Mice, Knockout; Microsatellite Repeats; Molecular Sequence Data; MutS Homolog 2 Protein; Mutation; Oxazolone/administration & dosage; Oxazolone/analogs & derivatives; Peyer's Patches; Proteins/genetics; Proteins/physiology; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/physiology
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.