Evidence map›Paper›PMID 27402226›Full record

ReviewTrends in immunology2016

T Cells Going Innate.

Midas Seyda, Abdallah Elkhal, Markus Quante, Christine S Falk, Stefan G Tullius

Abstract readReview
In one paragraph

Review in Trends in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-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

40 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Co-inhibitory profile and cytotoxicity of CD57Clinical and experimental immunology · 2018
    Trial
  3. Article
  4. Cytomegalovirus Drives the Development of Cytotoxic CD4Neurology(R) neuroimmunology & neuroinflammation · 2026
    Article
  5. Cationic mRNA Lipid Nanoparticles for Ex Vivo NanoCAR-T Cell Engineering.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Th17-driven CD8Cell death & disease · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Epigenetics behind CD8Genes and immunity · 2024
    Review
  12. Review
  13. Cigarette Smoke Modulates Inflammation and ImmunityAntioxidants & redox signaling · 2023
    Review
  14. Article
  15. [Analysis of the Efficacy of Immunotherapy in Elderly Patients with Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022
    Article
  16. Review
  17. Senescent CD4International journal of molecular sciences · 2022
    Review
  18. Review
  19. Review
  20. 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

5 authors at 3 institutions in 2 countries.

Midas SeydaDivision of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Institute of Transplant Immunology, IFB-Tx, Hannover Medical School, Hannover, Germany.
Abdallah ElkhalDivision of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Markus QuanteDivision of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Christine S FalkInstitute of Transplant Immunology, IFB-Tx, Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Hannover, Germany.
Stefan G TulliusDivision of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: stullius@partners.org.
Harvard University · USBrigham and Women's Hospital · USMedizinische Hochschule Hannover · DE

Funding

Consequences of Aging on Immune Response and Transplant OutcomeR01AG039449 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI TULLIUS, STEFAN GUNTHER · 2012 to 2016
$1.6M
NIA NIH HHS R01 AG039449
6 · The paper itself

Abstract

Natural killer (NK) cell receptors (NKRs) play a crucial role in the homeostasis of antigen-experienced T cells. Indeed, prolonged antigen stimulation may induce changes in the receptor repertoire of T cells to a profile that features NKRs. Chronic antigen exposure, at the same time, has been shown to trigger the loss of costimulatory CD28 molecules with recently reported intensified antigen thresholds of antigen-experienced CD8(+) T cells. In transplantation, NKRs have been shown to assist allograft rejection in a CD28-independent fashion. We discuss here a role for CD28-negative T cells that have acquired the competency of the NKR machinery, potentially promoting allorecognition either through T cell receptor (TCR) crossreactivity or independently from TCR recognition. Collectively, NKRs can bring about innate-like T cells by providing alternative costimulatory pathways that gain relevance in chronic inflammation, potentially leading to resistance to CD28-targeting immunosuppressants.

Indexed as

Immunity, InnateAdaptive ImmunityAgingAnimalsAntigensCD28 AntigensGene Expression RegulationHumansImmunosuppression TherapyInflammationKiller Cells, NaturalLymphocyte ActivationReceptors, Antigen, T-CellReceptors, Natural Killer CellSignal TransductionT-Lymphocyte SubsetsAntigensCD28 AntigensReceptors, Antigen, T-CellReceptors, Natural Killer Celladaptive immunityinnate immunityNK cell receptorsT cellstransplantation

Identifiers

PMID27402226
PMCPMC5633931
OpenAlexW2467858666

What OpenQuestion holds

Textmetadata
LicenceTDM
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.