Antibody diversity: a link between switching and hypermutation.
Recent work indicates that mutations in a cytidine deaminase homologue ablate both immunoglobulin class switch recombination and somatic hypermutation. These findings now explain cases of autosomal hyper-IgM syndrome and reveal that critical components for key functions of B cells require RNA editing.
Lieber
M
M
Departments of Pathology, Biochemistry, Microbiology and Biology, University of Southern California School of Medicine, Los Angeles, California 90098, USA. lieber@usc.edu
D000071479:APOBEC-1 Deaminase; D000916:Antibody Diversity; D003564:Cytidine Deaminase / Q000235:genetics / Q000378:metabolism*; D004247:DNA / Q000378:metabolism*; D014644:Genetic Variation; D006801:Humans; D017578:Immunoglobulin Class Switching; D017354:Point Mutation; D011946:Receptors, Antigen / Q000235:genetics*; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
D011946:Receptors, Antigen; D004247:DNA; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D000071479:APOBEC-1 Deaminase; C000605089:APOBEC1 protein, human; D003564:Cytidine Deaminase