Journal ArticleDOI
Anti-immunoglobulins induce death by apoptosis in WEHI-231 B lymphoma cells.
TLDR
It is shown that anti‐mIg treatment causes DNA fragmentation (apoptosis) in immature B lymphocytes such as WEHI‐231 cells, and co‐treatment with the protein kinase C activator phorbol 12‐myristate 13‐acetate prevents apoptosis induced by anti‐ mIg.Abstract:
Anti-membrane immunoglobulin (anti-mIg) antibodies exert inhibitory effects in immature B lymphocytes such as WEHI-231 cells. We show here that anti-mIg treatment causes DNA fragmentation (apoptosis) in these cells. We also report that co-treatment with the protein kinase C activator phorbol 12-myristate 13-acetate prevents apoptosis induced by anti-mIg. These results are in agreement with our initial proposal that sensitivity to the toxic effects of anti-mIg reflects, at least partially, altered signal transduction in immature B lymphocytes. Variations in signal transduction pathways during B lymphocyte ontogeny may, therefore, play a critical role in determining whether B cells should be activated or inhibited via their mIg.read more
Citations
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Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death.
TL;DR: The results suggest that activation of the PD‐1 gene may be involved in the classical type of programmed cell death.
Journal ArticleDOI
Clonal selection and learning in the antibody system
TL;DR: A second selection process occurs during immune responses in which a new antibody repertoire is generated through somatic hypermutation, where only mutants binding antigen with high affinity survive to become memory cells.
Journal ArticleDOI
Apoptosis: the biochemistry and molecular biology of programmed cell death.
TL;DR: This review first briefly covers some historical perspective on the discovery of apoptotic cell death, the characteristic morphology that accompanies this process, and the numerous cell types and mediators with which programmed cell death is associated.
Journal ArticleDOI
Toward an understanding of the molecular mechanisms of physiological cell death.
TL;DR: The ability of bcl-2 to protect cells from a wide variety of pathological, as well as physiological, stimuli indicates that many triggers can serve to activate the same suicide pathway, even some thought to cause necrosis, and not physiological cell death.
Journal ArticleDOI
Inhibition of NF-kappaB/Rel induces apoptosis of murine B cells.
Min Wu,Hayyoung Lee,Robert E. Bellas,Stephanie L. Schauer,Marcello Arsura,Douglas I. Katz,M J FitzGerald,Thomas L. Rothstein,David H. Sherr,Gail E. Sonenshein +9 more
TL;DR: Findings indicate that the drop in NF‐kappaB/Rel binding following anti‐IgM treatment activates apoptosis of WEHI 231 cells; furthermore, they implicate the NF‐ kappaB‐alpha‐GST protein or a c‐Rel affinity‐purified antibody induced apoptosis.
References
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Journal Article
Glucocorticoid activation of a calcium-dependent endonuclease in thymocyte nuclei leads to cell death.
J. John Cohen,Richard C. Duke +1 more
TL;DR: It appears that glucocorticoids cause thymocyte death by activating an enzyme that rapidly and extensively degrades DNA, and it is suggested that it may be part of a system for transporting calcium into the nucleus.
Journal ArticleDOI
Antibodies to CD3/T-cell receptor complex induce death by apoptosis in immature T cells in thymic cultures.
TL;DR: It is shown that engaging the CD3/TCR complex of immature mouse thymocytes with anti-CD3 antibodies produces DNA degradation and cell death through the endogenous pathway of apoptosis.
Journal ArticleDOI
Mechanism of antigen-driven selection in germinal centres.
Yong-Jun Liu,Douglas E. Joshua,Gwyn T. Williams,Christopher A. Smith,John Gordon,I. C. M. Maclennan +5 more
TL;DR: It is found that, on culture, centrocytes isolated from human tonsil kill themselves within a few hours by apoptosis, not a feature of other tonsillar B cells.
Journal ArticleDOI
Clonal deletion of B lymphocytes in a transgenic mouse bearing anti-MHC class I antibody genes
David Nemazee,Kurt Bürki +1 more
TL;DR: B-cell tolerance in transgenic mice using genes for IgM anti-H–2k MHC class I antibody is studied and it is suggested that very large numbers of autospecific B cells can be controlled by clonal deletion.
Journal ArticleDOI
Induction of self-tolerance in mature peripheral B lymphocytes
TL;DR: Identical changes in antigen-receptor expression occur in a subset of follicular B cells in nontransgenic mice, suggesting that clonally silenced self-reactive cells are common in the peripheral B-cell repertoire.