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The Journal of Immunology, 1998, 161: 6128-6132.
Copyright © 1998 by The American Association of Immunologists

Isolated Human Germinal Center Centroblasts Have an Intact Mismatch Repair System1

Kyoungsook Park2, Jaehoon Kim, Han-Soo Kim and Hyun S. Shin3

Molecular Immunology Laboratory, Samsung Biomedical Research Institute, Seoul, Korea

Ig somatic hypermutation contributes to the generation of high-affinity Abs that are essential for efficient humoral defense. The presence of multiple point mutations in rearranged Ig V genes and their immediate flanking sequences suggests that the DNA repair system may not be working properly in correcting point mutations introduced to the restricted region of Ig genes. We examined the DNA repair functions of germinal center (GC) centroblasts, which are the cells in which ongoing Ig hypermutation takes place. We found that GC centroblasts express all known components of the human DNA mismatch repair system, and that the system corrects DNA mismatches in a strand-specific manner in vitro. We conclude that general suppression of mismatch repair at the cellular level does not occur during somatic hypermutation.




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C. E. Schrader, W. Edelmann, R. Kucherlapati, and J. Stavnezer
Reduced Isotype Switching in Splenic B Cells from Mice Deficient in Mismatch Repair Enzymes
J. Exp. Med., August 2, 1999; 190(3): 323 - 330.
[Abstract] [Full Text] [PDF]


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N. Kim, G. Bozek, J. C. Lo, and U. Storb
Different Mismatch Repair Deficiencies All Have the Same Effects on Somatic Hypermutation: Intact Primary Mechanism Accompanied by Secondary Modifications
J. Exp. Med., July 5, 1999; 190(1): 21 - 30.
[Abstract] [Full Text] [PDF]




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