Evidence map›Paper›PMID 22652417›Full record

ArticleCytokine2012

CXCL10 contributes to p38-mediated apoptosis in primary T lymphocytes in vitro.

Abubaker M E Sidahmed, Alberto J León, Steven E Bosinger, David Banner, Ali Danesh, Mark J Cameron, David J Kelvin

Open access · hybridAbstract read
In one paragraph

Article in Cytokine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Extracellular vesicle storm during the course of Ebola virus infection in primates.Frontiers in cellular and infection microbiology · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Survival of Stem Cells and Progenitors in the Intestine Is Regulated by LPACellular and molecular gastroenterology and hepatology · 2022
    Article
  12. Role of CXCL10 in Spinal Cord Injury.International journal of medical sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  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

7 authors at 4 institutions in 3 countries.

Abubaker M E SidahmedDivision of Experimental Therapeutics, Toronto General Research Institute, Toronto, Ontario, Canada.
Alberto J León
Steven E Bosinger
David Banner
Ali Danesh
Mark J Cameron
David J Kelvin
Toronto General Hospital · CAShantou University · CNShantou University Medical College · CNUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

CXCL10 is part of the group of interferon-stimulated genes and it plays an important role during different viral infections by inducing cell activation, chemotaxis and lymphocyte priming toward the Th1 phenotype. In this study, we investigated in vitro the effects of CXCL10 in activated human primary T lymphocytes in terms of apoptosis or survival, and delineated the signaling pathways that are involved. CXCL10, in combination with IL-2 and/or IFNα, induces apoptosis in T lymphocytes. Moreover, CXCL10-induced activation of CXCR3 also triggers pro-survival signals that can be blocked by pertussis toxin. The analysis of the downstream signaling kinases shows that apoptosis is p38 MAPK-dependent and the pro-survival signals rely on the sustained activation of PI3K and the transient activation of Akt. On the other hand, the transient activation of p44/p42 ERK did not have an impact on T lymphocyte survival. We propose an immunological model in which CXCL10, together with other co-stimulating cytokines, participates in the activation of T lymphocytes, promotes survival and expansion of certain lymphocyte subsets, and induces chemotaxis toward the infected tissues. On the other hand, CXCL10 might contribute to the triggering of apoptosis in other subsets of T lymphocytes, including those lymphocytes that were transiently activated but later lacked the appropriate sets of specific co-stimulating signals to ensure their survival.

Indexed as

ApoptosisAdultCaspase 3Cells, CulturedCell SurvivalChemokine CXCL10Enzyme ActivationExtracellular Signal-Regulated MAP KinasesHumansInterferon-alphaInterleukin-2p38 Mitogen-Activated Protein KinasesPhosphorylationProto-Oncogene Proteins c-aktReceptors, CXCR3Recombinant ProteinsCaspase 3Chemokine CXCL10CXCR3 protein, humanExtracellular Signal-Regulated MAP KinasesInterferon-alphaInterleukin-2p38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktReceptors, CXCR3Recombinant Proteins

Identifiers

PMID22652417
PMCPMC7129786
OpenAlexW1995078506

What OpenQuestion holds

Textmetadata
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.