Evidence map›Paper›PMID 26185130›Full record

ArticleBlood2015

Dendritic cells accumulate in the bone marrow of myeloma patients where they protect tumor plasma cells from CD8+ T-cell killing.

Patrizia Leone, Simona Berardi, Maria Antonia Frassanito, Roberto Ria, Valli De Re, Sebastiano Cicco, Stefano Battaglia, Paolo Ditonno, Franco Dammacco, Angelo Vacca and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Article
  8. Review
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  15. Article
  16. T Cells Dysfunction in Multiple Myeloma.ImmunoTargets and therapy · 2025
    Review
  17. Review
  18. Efferocytosis and Bone Dynamics.Current osteoporosis reports · 2024
    Review
  19. Identification of Therapy-Induced Clonal Evolution and Resistance Pathways in Minimal Residual Clones in Multiple Myeloma through Single-Cell Sequencing.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  20. Article

25 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Patrizia LeoneDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Simona BerardiDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Maria Antonia FrassanitoDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Roberto RiaDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Valli De ReBio-Proteomics Facility, Department of Translational Research, Centro di Riferimento Oncologico, National Cancer Institute, Aviano, Italy; and.
Sebastiano CiccoDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Stefano BattagliaDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Paolo DitonnoHematology Unit, Di Venere Hospital, Bari, Italy.
Franco DammaccoDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Angelo VaccaDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
Vito RacanelliDepartment of Internal Medicine and Clinical Oncology, University of Bari Medical School, Bari, Italy;
University of Bari Aldo Moro · ITCentro di Riferimento Oncologico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many researchers have speculated that the clinical progression from monoclonal gammopathy of undetermined significance (MGUS) to multiple myeloma (MM) is driven by defects in dendritic cell (DC) function. However, evidence supporting this assumption is controversial, and no mechanism for the putative DC dysfunction has been demonstrated thus far. We studied DC subsets from the bone marrow of MM patients compared with those of MGUS patients and control subjects. We found that myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) accumulate in the bone marrow during the MGUS-to-MM progression. After engulfment of apoptotic tumor plasma cells via CD91, bone marrow mDCs and pDCs mature and are able to activate tumor-specific CD8(+) T cells. However, by interacting directly with CD28 on live (nonapoptotic) tumor plasma cells, bone marrow mDCs downregulate the expression of proteasome subunits in these cells, thus enabling their evasion from human leukocyte antigen (HLA) class I-restricted CD8(+) T-cell killing. These results suggest that DCs play a dual, but opposing, role in MM: for one, DCs activate CD8(+) T cells against tumor plasma cells and, for the other, DCs protect tumor plasma cells from CD8(+) T-cell killing. This information should be taken into account in designing immunotherapy approaches to enhance immune surveillance in MGUS and to break down immune tolerance in MM.

Indexed as

Bone MarrowCD8-Positive T-LymphocytesCell DeathCells, CulturedDendritic CellsHumansMultiple MyelomaPlasma CellsPlasmacytomaTumor Cells, Cultured

Identifiers

PMID26185130
PMCPMC4592278
OpenAlexW880640307

What OpenQuestion holds

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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.