2009
DOI: 10.1182/blood-2009-03-211763
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AID constrains germinal center size by rendering B cells susceptible to apoptosis

Abstract: IntroductionA fundamental hallmark of humoral immunity is the ability to produce class-switched antibodies that have enhanced affinity for antigen. This process, termed affinity maturation, allows clonally selected B cells to refine their response to theoretically target any antigen with high specificity. After activation, B cells mutate the immunoglobulin (Ig) locus in a process known as somatic hypermutation (SHM). 1 Mutated clones that have acquired increased affinity for antigen preferentially expand over … Show more

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Cited by 90 publications
(83 citation statements)
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“…[35][36][37][38] Immature B lymphocytes acquiring an excess number of nonproductive mutations undergo Fas-mediated apoptosis. 39,40 It is tempting to speculate that the coupling of these natural DNA DSB repair-inducing events with the global DNA damage accrued upon Artemis overexpression further sensitizes the cell to apoptotic stimuli. Consistent with this argument, the T lymphocyte population, which does not undergo somatic hypermutation or class switch recombination, was repopulated in EF1a-Artemistreated mice.…”
Section: Discussionmentioning
confidence: 99%
“…[35][36][37][38] Immature B lymphocytes acquiring an excess number of nonproductive mutations undergo Fas-mediated apoptosis. 39,40 It is tempting to speculate that the coupling of these natural DNA DSB repair-inducing events with the global DNA damage accrued upon Artemis overexpression further sensitizes the cell to apoptotic stimuli. Consistent with this argument, the T lymphocyte population, which does not undergo somatic hypermutation or class switch recombination, was repopulated in EF1a-Artemistreated mice.…”
Section: Discussionmentioning
confidence: 99%
“…A recent basic analysis has indicated increased proliferation and decreased apoptosis of AID ) ⁄ ) B lymphocytes in comparison with AID-expressing B lymphocytes derived from the GC. In addition, expression of AID was shown to lead to the generation of point mutations for SHM and CSR, resulting in DNA damage and apoptosis, (37) probably in the deregulated expression of anti-apoptotic factors such as bcl-2 and bcl-XL. (38) These findings suggest that cell-cycle arrest or apoptosis can be ultimately induced when sufficient AID is subsequently expressed in B lymphocytes after CSR.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, we could assume that these cells should undergo apoptosis once leaving the pseudo-follicles. A recent work suggesting a link between AID expression and B-cell apoptosis in GC favour this view [56]. In these conditions, the IgG pos subset could reflect the existence of an active microenvironment leading to permanent stimulation of the IgM pos pool, which would be turn on the CSR machinery maintaining this IgG pos subset in the PB.…”
Section: Proliferative Aid Positive Cll B-cellsmentioning
confidence: 97%