Activation-induced cell death in B lymphocytes

Donjerković, Dubravka; Scott, David W.

doi:10.1038/sj.cr.7290047

Cited by 83 publications

(73 citation statements)

References 71 publications

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“…This situation is thought to occur in immunity against polioviruses, where B cell memory against conformational epitopes is central to protection but requires support by T cells that recognize peptides from either internal or external capsid proteins [30,31]. On the other hand, there may be other explanations for this phenomenon; for example, it is known that strong immune-activation signals can induce lymphocyte apoptosis [32]. Linear epitopes of VP2 can elicit a strong initial IgG response, and it is conceivable that such stimulation could induce B cell apoptosis; however, this scenario seems unlikely, given that no loss of memory is observed in immunized mice.…”

Section: Discussionmentioning

confidence: 99%

B Cell Memory Is Directed toward Conformational Epitopes of Parvovirus B19 Capsid Proteins and the Unique Region of VP1

Corcoran¹,

Mahon²,

Doyle³

2004

J INFECT DIS

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Background. Loss of antibody reactivity against linear epitopes of parvovirus B19 (B19) capsid proteins VP1 and VP2 occurs after infection; however, it is unclear whether B cell memory is established against linear epitopes.Methods. B cell enzyme-linked immunospot assay was used to evaluate B19-specific B cell memory in volunteer donors ( ). n p 22 Results. B cell memory is maintained against conformational epitopes of VP2 and is absent against linear epitopes of VP2. Individuals seronegative for IgG against the unique region of VP1 have detectable B cell memory, with the potential to mount a humoral response on reexposure to B19. Conversely, in mice immunized with VP2, long-lasting IgG against linear epitopes of VP2 and a strong B cell-memory response are observed.Conclusions. B cell memory is established and maintained against conformational epitopes of VP2 and against linear epitopes of VP1 but not against linear epitopes of VP2. These findings further our understanding of the immune response to B19 and suggest that analysis of B19-specific B cell memory merits consideration for future B19-vaccine studies.

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Section: Discussionmentioning

confidence: 99%

B Cell Memory Is Directed toward Conformational Epitopes of Parvovirus B19 Capsid Proteins and the Unique Region of VP1

Corcoran¹,

Mahon²,

Doyle³

2004

J INFECT DIS

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“…Programmed cell death or apoptosis plays important roles in development of animals from C. elegans, Drosophila, to human, and is critical for the physiological function of many organs, such as the immune system [50][51][52][53]. Anuran metamorphosis is a postembryonic process that is absolutely dependent upon the presence of TH.…”

Section: Conclusion and Prospectsmentioning

confidence: 99%

Thyroid hormone regulation of apoptotic tissue remodeling during anuran metamorphosis

Shi

Hsia

et al. 2001

Cell Res

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Anuran metamorphosis involves systematic transformations of individual organs in a thyroid hormone (TH)-dependent manner. Morphological and cellular studies have shown that the removal of larval organs/ tissues such the tail and the tadpole intestinal epithelium is through programmed cell death or apoptosis. Recent molecular investigations suggest that TH regulates metamorphosis by regulating target gene expression through thyroid hormone receptors (TRs), which are DNA-binding transcription factors. Cloning and characterization of TH response genes show that diverse groups of early response genes are induced by TH. The products of these TH response genes are believed to directly or indirectly affect the expression and/or functions of cell death genes, which are conserved at both sequence and function levels in different animal species. A major challenge for future research lies at determining the signaling pathways leading to the activation of apoptotic processes and whether different death genes are involved in the regulation of apoptosis in different tissues/organs to effect tissue-specific transformations.

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“…When the speed of cell division exceeds that of cell death, an increase in the number of live cells after stimulation should be detected. In the literature, activation-induced cell death is triggered by BCR or CD40 signaling alone (32,33). Although CpG does not regulate mouse splenic B cell death, LPS is able to suppress cell apoptosis (33,34).…”

Section: Discussionmentioning

confidence: 99%

Decoy Receptor 3 Suppresses TLR2-Mediated B Cell Activation by Targeting NF-κB

Huang¹,

Kang²,

Chen³

et al. 2012

The Journal of Immunology

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Decoy receptor 3 (DcR3) is a soluble protein in the TNFR superfamily. Its known ligands include Fas ligand, homologous to lymphotoxin, showing inducible expression, and competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocytes, TNF-like molecule 1A, and heparan sulfate proteoglycans. DcR3 has been reported to modulate the functions of T cells, dendritic cells, and macrophages; however, its role in regulating B cell activation is largely unknown. In this study, we found that the DcR3.Fc fusion protein bound to human and mouse B cells and suppressed the activation of B cells. DcR3.Fc attenuated Staphylococcus aureus, IgM-, Pam3CSK4-, and LPS-mediated B cell proliferation but did not affect cytokine-induced B cell growth. In the presence of these mitogens, DcR3.Fc did not induce B cell apoptosis, suggesting that DcR3 may inhibit the signal(s) important for B cell activation. Because the combination of Fas.Fc, LT-βR.Fc (homologous to lymphotoxin, showing inducible expression, and competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocytes receptor), and DR3.Fc (TNF-like molecule 1A receptor) did not suppress B cell proliferation and because the biological effect of DcR3.Fc on B cells was not blocked by heparin, we hypothesize that a novel ligand(s) of DcR3 mediates its inhibitory activity on B cells. Moreover, we found that TLR2-stimulated NF-κB p65 activation and NF-κB–driven luciferase activity were attenuated by DcR3.Fc. The TLR2-induced cytokine production by B cells was consistently reduced by DcR3. These results imply that DcR3 may regulate B cell activation by suppressing the activation of NF-κB.

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Activation-induced cell death in B lymphocytes

Cited by 83 publications

References 71 publications

B Cell Memory Is Directed toward Conformational Epitopes of Parvovirus B19 Capsid Proteins and the Unique Region of VP1

B Cell Memory Is Directed toward Conformational Epitopes of Parvovirus B19 Capsid Proteins and the Unique Region of VP1

Thyroid hormone regulation of apoptotic tissue remodeling during anuran metamorphosis

Decoy Receptor 3 Suppresses TLR2-Mediated B Cell Activation by Targeting NF-κB

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