منابع مشابه
Signals that initiate somatic hypermutation of B cells in vitro.
Somatic hypermutation is initiated as B lymphocytes proliferate in germinal centers. The signals that switch on the mutation process are unknown. We have derived an in vitro system to define signals that will initiate mutation in normal, naive splenic B cells. We find that three signals are required to allow detection of somatic mutation in vitro; these are anti-Ig, anti-CD40, and anti-CD38. If...
متن کاملSomatic hypermutation in B cells: an optimal control treatment.
The vertebrate immune system generates high-affinity antibodies to external antigens through a process of somatic hypermutation that takes place in germinal centers formed in the secondary lymphoid tissues. B cells proliferating in these germinal centers experience random mutations in the genes encoding the variable region of their immunoglobulin molecules and are subsequently selected for high...
متن کاملTarget Somatic Hypermutation Identification of Core DNA Elements That
Somatic hypermutation (SHM) diversifies the V region of Ig genes and underlies the process of affinity maturation, in which B lymphocytes producing high-affinity Abs are generated and selected. SHM is triggered in activated B cells by deamination of deoxycytosine residues mediated by activation-induced deaminase (AID). Whereas mistargeting of SHM and AID results in mutations and DNA damage in m...
متن کاملSomatic hypermutation signature in B-cell low-grade lymphomas.
BACKGROUND Immunoglobulin gene somatic hypermutation is a biologically relevant and clinically useful prognostic factor in different types of low-grade B-cell lymphomas, including chronic lymphocytic leukemia, mantle cell lymphoma and splenic marginal zone lymphoma. DESIGN AND METHODS With the aim of identifying surrogate markers of somatic hypermutation, a combined investigation of IgV(H) mu...
متن کاملTLR ligation triggers somatic hypermutation in transitional B cells inducing the generation of IgM memory B cells.
TLR9 activation by unmethylated CpG provides a homeostatic mechanism to maintain B cell memory in the absence of Ag. In this study, we demonstrate that CpG also triggers the generation of somatically mutated memory B cells from immature transitional B cells. In response to CpG, a fraction of transitional B cells proliferates and introduces somatic hypermutations in the H chain V regions. The no...
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ژورنال
عنوان ژورنال: The Journal of Immunology
سال: 2001
ISSN: 0022-1767,1550-6606
DOI: 10.4049/jimmunol.166.4.2228