Mice and humans with inactivating mutations in the gene encoding activation-induced cytidine deaminase (AID) have an immunodeficiency disease known as 'hyper IgM type 2'. Since AID is the enzyme that catalyzes the conversion of cytosines in the DNA to uracils, thereby initiating the process of somatic hypermutation, why do individuals with this deficiency only produce IgM antibodies?
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