Evidence map›Paper›PMID 25250025›Full record

ArticleFrontiers in immunology2014

A Novel Prothrombotic Pathway in Systemic Sclerosis Patients: Possible Role of Bisphosphonate-Activated γδ T Cells.

Victoria Marcu-Malina, Alexandra Balbir-Gurman, Rima Dardik, Yolanda Braun-Moscovici, Michael J Segel, Ilan Bank

Open access · goldAbstract read
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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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  9. Increased CD14+ and decreased CD14- populations of monocytes 48 h after zolendronic acid infusion in breast cancer patients.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2017
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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

6 authors at 2 institutions in 1 country.

Victoria Marcu-MalinaLaboratory of Immunoregulation, Sheba Medical Center , Ramat Gan , Israel.
Alexandra Balbir-GurmanB Shine Rheumatology Unit, Rambam Health Care Campus, Rambam Medical Center , Haifa , Israel.
Rima DardikInstitutes of Thrombosis and Hemostasis, Sheba Medical Center , Ramat Gan , Israel.
Yolanda Braun-MoscoviciB Shine Rheumatology Unit, Rambam Health Care Campus, Rambam Medical Center , Haifa , Israel.
Michael J SegelInstitute of Pulmonary Diseases, Sheba Medical Center , Ramat Gan , Israel.
Ilan BankLaboratory of Immunoregulation, Sheba Medical Center , Ramat Gan , Israel ; Department of Medicine F, Sheba Medical Center , Ramat Gan , Israel ; Department of Medicine, Sackler School of Medicine, Tel Aviv University , Tel Aviv , Israel.
Sheba Medical Center · ILRambam Health Care Campus · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesInfusions of aminobisphonates (ABP) activate Vγ9δ2T cells in vivo and induce an acute inflammatory response in 30% of patients treated for osteoporosis. Following the observation of digital thrombosis in a systemic sclerosis (SSc) patient after treatment with an intravenous ABP, zoledronate (Zol), we evaluated whether patient and control peripheral blood (PB) mononuclear cell (MC, PBMC) acquire a prothrombotic phenotype in response to Zol.

resultsVγ9δ2T cells of both patients and healthy donors (HD) upregulated the CD69 activation antigen and secreted tumor necrosis factor (TNF)α in response to Zol in vitro. In addition, exposure to either Zol or lipopolysaccharide (LPS), or to both additively, induced expression of the highly procoagulant, tissue factor (TF)-1 on CD14+ monocytes. Importantly, only Zol-induced TF-1 was blocked by a monoclonal antibody to TNFα. Interestingly, we found that SSc, but not HD, Vδ1+ T cells were concurrently activated by Zol to produce interleukin (IL)-4. Addition of plasma from the blood of the SSc patient who developed critical digital ischemia after infusion of Zol, but neither plasma from a second patient with no adverse clinical response to Zol infusion nor of a HD, strongly enhanced Zol-induced monocyte TF-1, which could still be blocked by anti-TNFα.

conclusionAminobisphonates induced secretion of TNFα by Vγ9δ2+ T cells may lead to TNFα-dependent induction of procoagulant TF-1 induction on monocytes. In certain clinical settings, e.g., SSc, TF-1+ monocytes could play a role in triggering clinically relevant thrombosis.

Indexed as

aminobisphosphonatesclerodermaT cellsthrombosistissue factorVγ9δ2 T cellsγδ T cell

Identifiers

PMID25250025
PMCPMC4157565
OpenAlexW2062372633

What OpenQuestion holds

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Registered trials

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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.