Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the hyper-IgM syndrome (HIGM2)

Article Abstract:

Research reveals that cytidine deaminase gene mutation in association with the autosomal recessive form of hyper-IgM syndrome blocks IgG class switch recombination, IgG somatic hypermutations, and lymph node hyperplasia. Data indicate that cytidine deaminase is required for B cell terminal differentiation steps that confers affinity maturation of antibody responses.

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Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme

Article Abstract:

Results reveal that cytidine deaminase deficiency results in blocking class switch recombination process in B cells as well as somatic hypermutation in immunized cytidine deaminase deficient B cells. Data indicate that a common molecular mechanism controls the DNA modification step of both the processes.

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A novel cytidine deaminase affects antibody diversity

Article Abstract:

This review discusses the mechanistic aspects of antibody diversity brought about by cytidine deaminase. Data demonstrate that the enzyme influences both class switch recombination and the somatic hypermutation, which in turn alter the constant and variable regions of the antibody, respectively.

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