Abstract
Pharmacological manipulation of AID.
Highlights
In order to have an efficient humoral immune response, activated B lymphocytes with weak B cell receptor affinity for cognate antigen must undergo secondary antibody diversification
Active nuclear import of Activation induced deaminase (AID) is counteracted by a mechanism of cytoplasmic retention [1], and nuclear AID is exported back to the cytoplasm via the CRM1 carrier, so that a fraction of AID constantly shuttles between these two compartments [2]
Cytoplasmic AID has a significantly longer half-life than nuclear AID [3, 4] because the HSP90 molecular chaperoning pathway protects cytoplasmic AID [3] while a fraction of nuclear AID is targeted for rapid proteasomal degradation [4]
Summary
In order to have an efficient humoral immune response, activated B lymphocytes with weak B cell receptor affinity for cognate antigen must undergo secondary antibody diversification. Off-target AID activity can be pathogenic by mutating outside the Ig loci. Several mechanisms regulate AID and can limit its pathogenic potential. Even though the physiological target of AID is inside the nucleus, several mechanisms promote a predominantly cytoplasmic localization.
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