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?

Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
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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?
Transcribed Image Text: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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