B lymphocytes are resistant to death receptor 5-induced apoptosis

Crowder, Roslyn N.; Chatham, W. Winn; Zhou, Tong; Carter, Robert H.

doi:10.1016/j.clim.2010.12.006

Cited by 4 publications

(5 citation statements)

References 65 publications

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“…These results together suggest the potential to prevent auto-reactive B cells via modulation of the components in the inflammatory CD4-M1 pathogenic circuit. Consistent with the results we found in RA subjects [5] and previous report [32], we have analyzed peripheral blood mononuclear cells (PBMCs) from patients with SLE and have identified that treatment with TRA-8 resulted in elimination of CD4 T cells, but not CD19 B cells (Hsu et al, unpublished observations). These results suggested that consistent with results obtained from mice and human RA, CD4 T cells, but not B cells from SLE patients could be depleted by TRA-8 therapy.…”

Section: Introductionsupporting

confidence: 87%

The Dynamic Duo–Inflammatory M1 macrophages and Th17 cells in Rheumatic Diseases

Hsu

Mountz

2013

J Orth Rheumatol

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The synovial tissue of Rheumatoid Arthritis (RA) patients is enriched with macrophages and T lymphocytes which are two central players in the pathogenesis of RA. Interaction between myeloid cells and T cells are essential for the initiation and progression of the inflammatory processes in the synovium. With the rapid evolution of our understanding of how these two cell types are involved in the regulation of immune responses, RA is emerging as an ideal disease model for investigating the cell-cell interactions and consequently introducing novel biologic agents that are designed to disrupt these processes. This review will discuss the bidirectional interaction between the IL-23+ inflammatory macrophages and IL-17+ GM-CSF+ CD4 T cells in rheumatic diseases as well as potential antirheumatic strategies via apoptosis induction in this context.

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Section: Introductionsupporting

confidence: 87%

The Dynamic Duo–Inflammatory M1 macrophages and Th17 cells in Rheumatic Diseases

Hsu

Mountz

2013

J Orth Rheumatol

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“…In humans, TRAIL expression was described on various different innate and adaptive immune cell types including monocytes, macrophages, natural killer (NK) cells, T cells and B cells (23–26). TRAIL-R expression has been described in central and peripheral T cells and naïve and memory B cells upon activation (27, 28). While several non-transformed human cell types express TRAIL-Rs, many are refractory to the pro-apoptotic function of the ligand.…”

Section: Introductionmentioning

confidence: 99%

“…Nevertheless, it has been shown that non-transformed cells can be sensitized to TRAIL-induced apoptosis by activating cues or viral infections (29–31). However, the results were depending on activation protocols and specific cellular subsets, leading to inconsistent conclusions (27, 28, 32, 33). A systematic description of TRAIL-Rs in human B cell subpopulations is missing, as well as a comprehensive analysis of the sensitivity of primary human B cells to TRAIL-induced apoptosis ex vivo and upon activation.…”

Section: Introductionmentioning

confidence: 99%

TRAIL-R1 and TRAIL-R2 Mediate TRAIL-Dependent Apoptosis in Activated Primary Human B Lymphocytes

et al. 2019

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The maintenance of B cell homeostasis requires a tight control of B cell generation, survival, activation, and maturation. In lymphocytes upon activation, increased sensitivity to apoptotic signals helps controlling differentiation and proliferation. The death receptor Fas is important in this context because genetic Fas mutations in humans lead to an autoimmune lymphoproliferative syndrome that is similar to lymphoproliferation observed in Fas-deficient mice. In contrast, the physiological role of TNF-related apoptosis-inducing ligand receptors (TRAIL-Rs) in humans has been poorly studied so far. Indeed, most studies have focused on tumor cell lines and on mouse models whose results are difficult to transpose to primary human B cells. In the present work, the expression of apoptosis-inducing TRAIL-R1 and TRAIL-R2 and of the decoy receptors TRAIL-R3 and TRAIL-R4 was systematically studied in all developmental stages of peripheral B cells isolated from the blood and secondary lymphoid organs. Expression of TRAIL-Rs is modulated along development, with highest levels observed in germinal center B cells. In addition, T-dependent and T-independent signals elicited induction of TRAIL-Rs with distinct kinetics, which differed among B cell subpopulations: switched memory cells rapidly upregulated TRAIL-R1 and -2 upon activation while naïve B cells only reached similar expression levels at later time points in culture. Increased expression of TRAIL-R1 and -2 coincided with a caspase-3-dependent sensitivity to TRAIL-induced apoptosis in activated B cells but not in freshly isolated resting B cells. Finally, both TRAIL-R1 and TRAIL-R2 could signal actively and both contributed to TRAIL-induced apoptosis. In conclusion, this study provides a systematic analysis of the expression of TRAIL-Rs in human primary B cells and of their capacity to signal and induce apoptosis. This dataset forms a basis to further study and understand the dysregulation of TRAIL-Rs and TRAIL expression observed in autoimmune diseases. Additionally, it will be important to foresee potential bystander immunomodulation when TRAIL-R agonists are used in cancer treatment.

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“…Upregulation of TRAIL on human B cells was seen with IFNα and IFNα-inducers, like TLR9 ligands [51], but not following stimulation via the BCR, PHA/IL-2, or IFNβ [51,53]. Furthermore, naïve B cells expressed DR4 [27,239,240] and DR5 [32,239,240,241] and their expression levels increased upon stimulation [239,240,242]. Consequently, germinal center (GC) or memory B cells expressed higher levels of DR4 and DR5 than naïve cells [239,240].…”

Section: Expression and Function Of Trail/drs In Immune Cellsmentioning

confidence: 99%

The Role of TRAIL/DRs in the Modulation of Immune Cells and Responses

Sağ

Ayyildiz

Gunalp

et al. 2019

Cancers

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Expression of TRAIL (tumor necrosis factor–related apoptosis–inducing ligand) by immune cells can lead to the induction of apoptosis in tumor cells. However, it becomes increasingly clear that the interaction of TRAIL and its death receptors (DRs) can also directly impact immune cells and influence immune responses. Here, we review what is known about the role of TRAIL/DRs in immune cells and immune responses in general and in the tumor microenvironment in particular.

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B lymphocytes are resistant to death receptor 5-induced apoptosis

Cited by 4 publications

References 65 publications

The Dynamic Duo–Inflammatory M1 macrophages and Th17 cells in Rheumatic Diseases

The Dynamic Duo–Inflammatory M1 macrophages and Th17 cells in Rheumatic Diseases

TRAIL-R1 and TRAIL-R2 Mediate TRAIL-Dependent Apoptosis in Activated Primary Human B Lymphocytes

The Role of TRAIL/DRs in the Modulation of Immune Cells and Responses

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