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GENES & DEVELOPMENT 18:1-11, 2004
©2004 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
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REVIEW

The generation of antibody diversity through somatic hypermutation and class switch recombination

Ziqiang Li1, Caroline J. Woo1, Maria D. Iglesias-Ussel, Diana Ronai and Matthew D. Scharff2

Department of Cell Biology, Albert Einstein College of Medicine, New York, New York 10461, USA

The first 100 words of the full text of this article appear below.

Antibody-mediated immunity is critical to the resistance of vertebrate species to pathogenic organisms. Although low-affinity immunoglobin (Ig) M antibodies circulate in the blood prior to encountering pathogens, high-affinity IgG and IgA antibodies are required to inactivate toxins, neutralize viruses, and promote the clearance of microorganisms. Individuals, such as those with hyper-IgM syndrome (HIGM), who lack the ability to make such high-affinity IgG and IgA antibodies, are unable to combat bacterial and viral infections and usually die at a young age (Revy et al. 2000Go; Imai et al. 2003Go). Prior to exposure to antigen, the initial generation of a . . . [Full Text of this Article]


    The characteristics of SHM
 

    Characteristics of class switch recombination
 

    Molecules involved in SHM and CSR
 

Activation-induced cytidine deaminase


Uracil N-glycosylase


Mismatch repair proteins


Error-prone DNA polymerases


Nonhomologous end joining


    Model for the production of mutations in both SHM and CSR
 

    Is MMR playing a direct or indirect role in SHM and CSR?
 

    How is AID targeted to the V and S regions but not to other genes?
 

What is the role of transcription in SHM and CSR?


Are there cis-acting sequences that target AID for mutations?


Does chromatin structure play a role in the targeting of SHM and CSR?


    Future Direction
 

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