What is B cell hypermutation?

What is B cell hypermutation?

Definition. Somatic hypermutation is a process that allows B cells to mutate the genes that they use to produce antibodies. This enables the B cells to produce antibodies that are better able to bind to bacteria, viruses and other infections.

What do you mean by somatic hypermutation?

Somatic hypermutation (or SHM) is a cellular mechanism by which the immune system adapts to the new foreign elements that confront it (e.g. microbes), as seen during class switching.

What is the importance of somatic hypermutation?

Somatic hypermutation (SHM) of immunoglobulin (Ig) genes plays a key role in antibody mediated immunity. SHM in B cells provides the molecular basis for affinity maturation of antibodies. In this way SHM is key in optimizing antibody dependent immune responses.

Do plasma cells undergo somatic hypermutation?

The germinal centre B cells undergo somatic hypermutation and class switch recombination. Plasma cells and memory B cells with a high-affinity for the original antigen stimuli are produced. These cells are long lived and plasma cells may secrete antibody for weeks after the initial infection.

What triggers somatic hypermutation?

Hypermutation is triggered by activation-induced deaminase (AID), an enzyme which catalyzes targeted deamination of deoxycytidine residues in DNA. The pathways used for processing the AID-generated U:G lesions determine the variety of base substitutions observed during somatic hypermutation.

Where does somatic hypermutation occur in the body?

Somatic hypermutation only happens in activated B cells, and not in T cells. This happens at sites where B cells are activated and T cells are also present- basically in germinal centers within lymph nodes and the spleen. When B cells receive antigen stimulation by crosslinking their BCRs, they express the molecule CD40 on their surface.

Why does aid lead to somatic hypermutation and affinity maturation?

In addition to promoting class switching, AID also leads to somatic hypermutation. You see, AID can only bind to single-stranded DNA, so it’s really only able to target genes that are being actively transcribed during the rapid proliferation phase that occurs following B cell activation.

What is the relationship between CSR and somatic hypermutation?

The relationship between class switch recombination (CSR) and somatic hypermutation has been unclear. By using human CD27 − naive B cells, we investigated the somatic hypermutation and producibility of immunoglobulins (Igs) that occur after CSR.

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