Journal
IMMUNITY
Volume 44, Issue 4, Pages 769-781Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2016.01.011
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Funding
- NIH Medical Scientist Training Program [T32GM07739]
- National Institute of Allergy and Infectious Diseases, NIH [1F30AI109903-01]
- National Center for Advancing Translational Sciences (NCATS), NIH Clinical and Translational Science Award program [UL1 TR000043]
- NIH [AI037526-19, AI072529-06]
- NIH Center for HIV/AIDS Vaccine Immunology and Immunogen Discovery (CHAVI-ID) [1UM1 AI100663-01]
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Somatic hypermutation (SHM) and class-switch recombination (CSR) increase the affinity and diversify the effector functions of antibodies during immune responses. Although SHM and CSR are fundamentally different, their independent roles in regulating B cell fate have been difficult to uncouple because a single enzyme, activation-induced cytidine deaminase (encoded by Aicda), initiates both reactions. Here, we used a combination of Aicda and antibody mutant alleles that separate the effects of CSR and SHM on polyclonal immune responses. We found that class-switching to IgG1 biased the fate choice made by B cells, favoring the plasma cell over memory cell fate without significantly affecting clonal expansion in the germinal center (GC). In contrast, SHM reduced the longevity of memory B cells by creating polyreactive specificities that were selected against over time. Our data define the independent contributions of SHM and CSR to the generation and persistence of memory in the antibody system.
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