Evidence map›Paper›PMID 25647836›Full record

ArticleBlood2015

CXCR4 expression on pathogenic T cells facilitates their bone marrow infiltration in a mouse model of aplastic anemia.

Christina Arieta Kuksin, Gabriela Gonzalez-Perez, Lisa M Minter

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. [Causal relationship between autoimmune diseases and aplastic anemia: A Mendelian randomization study].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  7. Review
  8. Article
  9. Directing the migration of serum-free,Frontiers in immunology · 2024
    Article
  10. Influence of Housing Temperature and Genetic Diversity on Allogeneic T Cell-Induced Tissue Damage in Mice.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. [Kinetics of immune activated T cells in aplastic anemia mouse model].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022
    Article
  15. Article
  16. Article
  17. Article
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  19. Article
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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

3 authors at 1 institution in 1 country.

Christina Arieta KuksinDepartment of Veterinary and Animal Sciences, and.
Gabriela Gonzalez-PerezDepartment of Veterinary and Animal Sciences, and.
Lisa M MinterDepartment of Veterinary and Animal Sciences, and Program in Molecular and Cellular Biology, University of Massachusetts Amherst, Amherst, MA.
University of Massachusetts Amherst · US

Funding

Targeting y-secretase in GVHDP01CA166009 · NCI · UNIVERSITY OF MASSACHUSETTS AMHERST · PI OSBORNE, BARBARA A · 2013 to 2017
$4.9M
NCI NIH HHS 1P01 CA166009-01A1NCI NIH HHS P01 CA166009
6 · The paper itself

Abstract

Aplastic anemia (AA) is a disease characterized by T-cell-mediated destruction of bone marrow (BM) hematopoietic stem and progenitor cells. Physiologically, T cells migrate to the BM in response to chemokines, such as SDF-1α, the ligand for CXCR4. However, how T cells traffic to the BM in AA is poorly understood. CXCR4 is aberrantly expressed in immune-mediated diseases and its regulation by nuclear factor-κB (NF-κB) in cancer models is well documented. In this study, we show that CXCR4 is highly expressed on BM-infiltrating CD4(+) and CD8(+) T cells in a mouse model of AA. Inhibiting CXCR4 in AA mice, using CXCR4(-/-) splenocytes or AMD3100, significantly reduced BM infiltration of T cells. We also report that NF-κB occupancy at the CXCR4 promoter is enhanced in BM-infiltrating CD8(+) T cells of AA mice. Moreover, inhibiting NF-κB signaling in AA mice using Bay11 or dehydroxymethylepoxyquinomicin, or transferring p50(-/-) splenocytes, decreased CXCR4 expression on CD8(+) T cells, significantly reduced BM infiltration of T cells, and strongly attenuated disease symptoms. Remarkably, therapeutic administration of Bay11 significantly extended survival of AA mice. Overall, we demonstrate that CXCR4 mediates migration of pathogenic T cells to the BM in AA mice, and inhibiting NF-κB signaling may represent a novel therapeutic approach to treating AA.

Indexed as

Anemia, AplasticChemotaxis, LeukocyteDisease Models, AnimalMiceAnimalsBone MarrowCD8-Positive T-LymphocytesFemaleHumansMaleMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutNF-kappa BReceptors, CXCR4CXCR4 protein, mouseNF-kappa BReceptors, CXCR4

Identifiers

PMID25647836
PMCPMC4375106
OpenAlexW2039696313

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.