Evidence map›Paper›PMID 24765093›Full record

ArticleFrontiers in immunology2014

Human B Cell-Derived Lymphoblastoid Cell Lines Constitutively Produce Fas Ligand and Secrete MHCII(+)FasL(+) Killer Exosomes.

Matthew W Klinker, Vincent Lizzio, Tamra J Reed, David A Fox, Steven K Lundy

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 91 citations in OpenAlex.

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  9. Extracellular vesicles in malignant and normal B lymphocyte growth and development.Extracellular vesicles and circulating nucleic acids · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Matthew W KlinkerGraduate Program in Immunology, University of Michigan , Ann Arbor, MI , USA ; Division of Rheumatology, Department of Internal Medicine, University of Michigan , Ann Arbor, MI , USA.
Vincent LizzioDivision of Rheumatology, Department of Internal Medicine, University of Michigan , Ann Arbor, MI , USA.
Tamra J ReedDivision of Rheumatology, Department of Internal Medicine, University of Michigan , Ann Arbor, MI , USA.
David A FoxGraduate Program in Immunology, University of Michigan , Ann Arbor, MI , USA ; Division of Rheumatology, Department of Internal Medicine, University of Michigan , Ann Arbor, MI , USA.
Steven K LundyGraduate Program in Immunology, University of Michigan , Ann Arbor, MI , USA ; Division of Rheumatology, Department of Internal Medicine, University of Michigan , Ann Arbor, MI , USA.
University of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune suppression mediated by exosomes is an emerging concept with potentially immense utility for immunotherapy in a variety of inflammatory contexts, including allogeneic transplantation. Exosomes containing the apoptosis-inducing molecule Fas ligand (FasL) have demonstrated efficacy in inhibiting antigen-specific immune responses upon adoptive transfer in animal models. We report here that a very high frequency of human B cell-derived lymphoblastoid cell lines (LCL) constitutively produce MHCII(+)FasL(+) exosomes that can induce apoptosis in CD4(+) T cells. All LCL tested for this study (>20 independent cell lines) showed robust expression of FasL, but had no detectable FasL on the cell surface. Given this intracellular sequestration, we hypothesized that FasL in LCL was retained in the secretory lysosome and secreted via exosomes. Indeed, we found both MHCII and FasL proteins present in LCL-derived exosomes, and using a bead-based exosome capture assay demonstrated the presence of MHCII(+)FasL(+) exosomes among those secreted by LCL. Using two independent experimental approaches, we demonstrated that LCL-derived exosomes were capable of inducing antigen-specific apoptosis in autologous CD4(+) T cells. These results suggest that LCL-derived exosomes may present a realistic source of immunosuppressive exosomes that could reduce or eliminate T cell-mediated responses against donor-derived antigens in transplant recipients.

Indexed as

Epstein–Barr viruskiller B cellslethal exosomesmicrovesiclesregulatory B cellsT cell apoptosistransplant tolerance

Identifiers

PMID24765093
PMCPMC3980107
OpenAlexW2141646454

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.