Evidence map›Paper›PMID 26174551›Full record

ArticleJournal of translational medicine2015

IL-17/IL-10 double-producing T cells: new link between infections, immunosuppression and acute myeloid leukemia.

Gerardo Musuraca, Serena De Matteis, Roberta Napolitano, Cristina Papayannidis, Viviana Guadagnuolo, Francesco Fabbri, Delia Cangini, Michela Ceccolini, Maria Benedetta Giannini, Alessandro Lucchesi and 10 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
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  5. Review
  6. Article
  7. Article
  8. The impact of blood Transfusion on T Helper Cells and Cytokines in Transfusion-Refractory Patients: a Prospective Study.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
    Article
  9. Review
  10. Review
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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

20 authors.

Gerardo MusuracaHematology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. gerardo.musuraca@irst.emr.it.
Serena De MatteisBiosciences Laboratory, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. serena.dematteis@irst.emr.it.
Roberta NapolitanoBiosciences Laboratory, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. roberta.napolitano@irst.emr.it.
Cristina PapayannidisDepartment of Hematology and Oncological Sciences 'L. and A. Seràgnoli', University of Bologna, Bologna, Italy. cristina.papayannidis@unibo.it.
Viviana GuadagnuoloDepartment of Hematology and Oncological Sciences 'L. and A. Seràgnoli', University of Bologna, Bologna, Italy. viviana.guadagnuolo2@unibo.it.
Francesco FabbriBiosciences Laboratory, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. francesco.fabbri@irst.emr.it.
Delia CanginiHematology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. delia.cangini@irst.emr.it.
Michela CeccoliniHematology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. michela.ceccolini@irst.emr.it.
Maria Benedetta GianniniHematology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. maria.giannini@irst.emr.it.
Alessandro LucchesiHematology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. alessandro.lucchesi@irst.emr.it.
Sonia RonconiHematology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. sonia.ronconi@irst.emr.it.
Paolo MariottiDepartment of Hematology and Oncological Sciences 'L. and A. Seràgnoli', University of Bologna, Bologna, Italy. paolo.mariotti5@unibo.it.
Paolo SaviniInternal Medicine Unit, Infermi Hospital, Faenza, Italy. p.savini@ausl.ra.it.
Monica TaniHaematology Unit, Santa Maria delle Croci Hospital, Ravenna, Italy. monica.tani@ausl.ra.it.
Pier Paolo FattoriHematology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. pierpaolo.fattori@irst.emr.it.
Massimo GuidoboniImmunotherapy Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. massimo.guidoboni@irst.emr.it.
Giovanni MartinelliDepartment of Hematology and Oncological Sciences 'L. and A. Seràgnoli', University of Bologna, Bologna, Italy. giovanni.martinelli2@unibo.it.
Wainer ZoliBiosciences Laboratory, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. wainer.zoli@irst.emr.it.
Dino AmadoriDepartment of Medical Oncology, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. dino.amadori@irst.emr.it.
Silvia CarloniBiosciences Laboratory, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. silvia.carloni@irst.emr.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) is an incurable disease with fatal infections or relapse being the main causes of death in most cases. In particular, the severe infections occurring in these patients before or during any treatment suggest an intrinsic alteration of the immune system. In this respect, IL-17-producing T helper (Th17) besides playing a key role in regulating inflammatory response, tumor growth and autoimmune diseases, have been shown to protect against bacterial and fungal pathogens. However, the role of Th17 cells in AML has not yet been clarified.

methodsT cell frequencies were assessed by flow cytometry in the peripheral blood of 30 newly diagnosed AML patients and 30 age-matched healthy volunteers. Cytokine production was determined before and after culture of T cells with either Candida Albicans or AML blasts. Statistical analyses were carried out using the paired and unpaired two-tailed Student's t tests and confirmed with the non parametric Wilcoxon signed-rank test.

resultsA strong increase of Th17 cells producing immunosuppressive IL-10 was observed in AML patients compared with healthy donors. In addition, stimulation of AML-derived T cells with a Candida albicans antigen induced significantly lower IFN-γ production than that observed in healthy donors; intriguingly, depletion of patient Th17 cells restored IFN-γ production after stimulation. To address the role of AML blasts in inducing Th17 alterations, CD4+ cells from healthy donors were co-cultured with CD33+ blasts: data obtained showed that AML blasts induce in healthy donors levels of IL-10-producing Th17 cells similar to those observed in patients.

conclusionsIn AML patients altered Th17 cells actively cause an immunosuppressive state that may promote infections and probably tumor escape. Th17 cells could thus represent a new target to improve AML immunotherapy.

Indexed as

Immunosuppression TherapyAdultAgedAged, 80 and overBlast CrisisCandida albicansCandidiasisCoculture TechniquesCytokinesFemaleHumansInterferon-gammaInterleukin-10Interleukin-17Leukemia, Myeloid, AcuteLymphocyte CountCytokinesInterferon-gammaInterleukin-10Interleukin-17Sialic Acid Binding Ig-like Lectin 3

Identifiers

PMID26174551
PMCPMC4502949

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