Evidence map›Paper›PMID 26286066›Full record

ArticleBMC nephrology2015

Effect of induction therapy on the expression of molecular markers associated with rejection and tolerance.

Eva Krepsova, Irena Tycova, Alena Sekerkova, Peter Wohlfahrt, Petra Hruba, Ilja Striz, Birgit Sawitzki, Ondrej Viklicky

Abstract read
In one paragraph

Article in BMC nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
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  8. Article
  9. T Cells With ActivatedFrontiers in immunology · 2022
    Article
  10. CD4Frontiers in immunology · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Article
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

8 authors.

Eva KrepsovaTransplant Laboratory, Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. eva.krepsova@ikem.cz.
Irena TycovaTransplant Laboratory, Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. irena.tycova@ikem.cz.
Alena SekerkovaDepartment of Clinical and Transplant Immunology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. alena.sekerkova@ikem.cz.
Peter WohlfahrtDepartment of Preventive Cardiology, Cardiology Centre, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. peter.wohlfahrt@ikem.cz.
Petra HrubaTransplant Laboratory, Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. petra.hruba@ikem.cz.
Ilja StrizDepartment of Clinical and Transplant Immunology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. ilja.striz@ikem.cz.
Birgit SawitzkiInstitute of Medical Immunology and Berlin-Brandenburg Centre for Regenerative Therapies (BCRT), Charité University Medicine, Berlin, Germany. birgit.sawitzki@charite.de.
Ondrej ViklickyTransplant Laboratory, Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. ondrej.viklicky@ikem.cz.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInduction therapy can improve kidney transplantation (KTx) outcomes, but little is known about the mechanisms underlying its effects.

methodsThe mRNA levels of T cell-related genes associated with tolerance or rejection (CD247, GZMB, PRF1, FOXP3, MAN1A1, TCAIM, and TLR5) and lymphocyte subpopulations were monitored prospectively in the peripheral blood of 60 kidney transplant recipients before and 7, 14, 21, 28, 60, 90 days, 6 months, and 12 months after KTx. Patients were treated with calcineurin inhibitor-based triple immunosuppression and induction with rabbit anti-thymocyte globulin (rATG, n = 24), basiliximab (n = 17), or without induction (no-induction, n = 19). A generalized linear mixed model with gamma distribution for repeated measures, adjusted for rejection, recipient/donor age and delayed graft function, was used for statistical analysis.

resultsrATG treatment caused an intense reduction in all T cell type population and natural killer (NK) cells within 7 days, then a slow increase and repopulation was observed. This was also noticed in the expression levels of CD247, FOXP3, GZMB, and PRF1. The basiliximab group exhibited higher CD247, GZMB, FOXP3 and TCAIM mRNA levels and regulatory T cell (Treg) counts than the no-induction group. The levels of MAN1A1 and TLR5 mRNA expressions were increased, whereas TCAIM decreased in the rATG group as compared with those in the no-induction group.

conclusionThe rATG induction therapy was associated with decreased T and NK cell-related transcript levels and with upregulation of two rejection-associated transcripts (MAN1A1 and TLR5) shortly after KTx. Basiliximab treatment was associated with increased absolute number of Treg cells, and increased level of FOXP3 and TCAIM expression.

Indexed as

AdultAgedAntibodies, MonoclonalAntilymphocyte SerumBasiliximabCalcineurin InhibitorsCD3 ComplexFemaleForkhead Transcription FactorsGene ExpressionGraft RejectionGranzymesHumansImmune ToleranceImmunosuppression TherapyImmunosuppressive AgentsAntibodies, MonoclonalAntilymphocyte SerumBasiliximabCalcineurin InhibitorsCD3 antigen, zeta chainCD3 ComplexForkhead Transcription FactorsFOXP3 protein, humanGranzymesGZMB protein, humanImmunosuppressive AgentsMannosidasesmannosyl-oligosaccharide 1,2-alpha-mannosidasePerforinPRF1 protein, humanRecombinant Fusion ProteinsRNA, Messenger

Identifiers

PMID26286066
PMCPMC4545708

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.