Hyperactivated B cells in human inflammatory bowel disease

Noronha, Ansu; Liang, Yanmei; Hetzel, Jeremy T.; Hastürk, Hatice; Kantarcı, Alpdoğan; Stucchi, Arthur F.; Zhang, Yue; Nikolajczyk, Barbara S.; Farraye, Francis A.; Ganley-Leal, Lisa

doi:10.1189/jlb.0309203

Cited by 68 publications

(72 citation statements)

References 59 publications

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“…However, after transplantation, a small amount of allogeneic PDLSCs might be presented to B cells as antigen by antigen-presenting cells, and these B cells might be stimulated and express IL-6 and B7, which activated the PD-1/PD-L1 expression of MSCs in periodontal tissue. Previous studies suggest that activated human B cells can circulate throughout the body [47], so the B cells in inflamed periodontal tissue can be existed in situ or migrated from lymph nodes and other inflammatory tissues. After treatment, the allogeneic MSCs migrated followed CXCL12, CXCL13, and CCL19 density [11,48] toward the site of inflamed area, suppressed the chemotaxis in B cells.…”

Section: Discussionmentioning

confidence: 99%

Periodontal Ligament Stem Cells Regulate B Lymphocyte Function via Programmed Cell Death Protein 1

Liu

Ding

et al. 2013

Stem Cells

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Periodontal ligament stem cells (PDLSCs) have provided novel cell sources for tooth and periodontal tissue regeneration. Allogeneic PDLSCs can reconstruct periodontal ligament tissue that has been damaged by periodontal diseases and regulate T-cell immunity. However, the effect of PDLSCs on B cells remains unknown. Here, we treated periodontitis in a miniature pig model using allogeneic PDLSCs and showed a reduction in humoral immunity in the animals. When cocultured with normal B cells, human PDLSCs (hPDLSCs) had similar effects as bone marrow mesenchymal stem cells in suppressing B cell proliferation, differentiation, and migration, while intriguingly, hPDLSCs increased B cell viability by secreting interleukin-6. Mechanistically, hPDLSCs suppressed B cell activation through cell-to-cell contact mostly mediated by programmed cell death protein 1 and programmed cell death 1 ligand 1. Our data revealed a previously unrecognized function of PDLSCs in regulating humoral immune responses, which may represent a novel therapeutic strategy for immune-related disorders.

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Section: Discussionmentioning

confidence: 99%

Periodontal Ligament Stem Cells Regulate B Lymphocyte Function via Programmed Cell Death Protein 1

Liu

Ding

et al. 2013

Stem Cells

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“…We thus assessed phospho (P)-kinases within the well-described BCR Ag capture signaling pathways for comparison with CD23 (20). Signaling through CD23 was similar in tonsil, peripheral blood, and Ramos B cells except for basal levels of P-ERK1/2, which we previously reported were higher in circulating B cells (22). AntiIgE, anti-CD23, and Ag-specific cross-linking of cell-bound IgE (Fig.…”

Section: Cd23mentioning

confidence: 92%

CD23-Bound IgE Augments and Dominates Recall Responses through Human Naive B Cells

Griffith

Liang

Onguru

et al. 2011

The Journal of Immunology

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Human peripheral blood BCRμ+ B cells express high levels of CD23 and circulate preloaded with IgE. The Ag specificity of CD23-bound IgE presumably differs from the BCR and likely reflects the Ag-specific mix of free serum IgE. CD23-bound IgE is thought to enhance B cell Ag presentation to T cells raising the question of how a B cell might respond when presented with a broad mix of Ags and CD23-bound IgE specificities. We recently reported that an increase in CD23+ B cells is associated with the development of resistance to schistosomiasis, highlighting the potential importance of CD23-bound IgE in mediating immunity. We sought to determine the relationship between BCR and CD23-bound IgE-mediated B cell activation in the context of schistosomiasis. We found that crude schistosome Ags downregulate basal B cell activation levels in individuals hyperexposed to infectious worms. Schistosome-specific IgE from resistant, occupationally exposed Kenyans recovered responses of B cells to schistosome Ag. Furthermore, cross-linking of CD23 overrode intracellular signals mediated via the BCR, illustrating its critical and dominating role in B cell activation. These results suggest that CD23-bound IgE augments and dominates recall responses through naive B cells.

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“…[19][20][21] These activated B cells can secrete significant amounts of cytokines and chemokines while in circulation. 19 However, systemic host-and microbial-derived TLR ligands can modify B-cell responses in a pro-or antiinflammatory manner. 22 This has been shown primarily by the differential responses of human B cells to TLR4 ligands.…”

mentioning

confidence: 99%

Human Schistosomiasis Is Associated with Endotoxemia and Toll-Like Receptor 2- and 4-Bearing B Cells

Onguru¹,

Liang²,

Griffith³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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Schistosomiasis is caused by parasitic trematodes. Individuals can accumulate hundreds of intravascular worms, which secrete a myriad of antigenic molecules into the bloodstream. Some of these molecules suppress immunity to microbial Toll-like receptor (TLR) ligands, such as lipopolysaccharides, which may increase host susceptibility to coinfecting pathogens. We show that schistosomiasis is associated with extremely high levels of endotoxemia as well as high mobility group 1, an endogenous inflammatory TLR ligand, in the absence of other coinfected pathogens. Circulating B cells express surface TLR2 and TLR4, reflecting systemic exposure to microbial ligands. Bacterial translocation may occur with schistosomal egg movement from the vascular to the gut and other routes, such as the skin during infection. Our report suggests that immunosuppressive schistosome antigens may have evolved to curb inflammatory responses to the high antigenic burden of translocated bacteria products and endogenous TLR ligands that arise during parasite exposure and inflammation.

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Hyperactivated B cells in human inflammatory bowel disease

Cited by 68 publications

References 59 publications

Periodontal Ligament Stem Cells Regulate B Lymphocyte Function via Programmed Cell Death Protein 1

Periodontal Ligament Stem Cells Regulate B Lymphocyte Function via Programmed Cell Death Protein 1

CD23-Bound IgE Augments and Dominates Recall Responses through Human Naive B Cells

Human Schistosomiasis Is Associated with Endotoxemia and Toll-Like Receptor 2- and 4-Bearing B Cells

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