Evidence map›Paper›PMID 19265119›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Lymphocytes with aberrant expression of Fas or Fas ligand attenuate immune bone marrow failure in a mouse model.

Stephanie O Omokaro, Marie J Desierto, Michael A Eckhaus, Felicia M Ellison, Jichun Chen, Neal S Young

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  8. Deficit of circulating CD19British journal of haematology · 2020
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  15. Allogeneic Th1 cells home to host bone marrow and spleen and mediate IFNγ-dependent aplasia.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2013
    Article
  16. Article
  17. Hydrogen therapy may be an effective and specific novel treatment for aplastic anemia.Medical science monitor : international medical journal of experimental and clinical research · 2012
    Article
  18. Article
  19. 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

6 authors at 2 institutions in 1 country.

Stephanie O OmokaroHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda,MD 20892, USA. omokaros@mail.nih.gov
Marie J Desierto
Michael A Eckhaus
Felicia M Ellison
Jichun Chen
Neal S Young
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

Bone marrow (BM) and lymphocyte samples from aplastic anemia patients show up-regulated Fas and Fas-ligand (FasL) expression, respectively, supporting a relationship between immune-mediated BM destruction and the Fas apoptotic pathway. Mice with spontaneous lymphoproliferation (lpr) and generalized lymphoproliferative disease (gld) mutations exhibit abnormal expression of Fas and FasL, serving as potential models to elucidate underlying mechanisms of BM failure. We examined cellular and functional characteristics of lpr and gld mutants on the C57BL/6 (B6) background. Lymph node (LN) cells from lpr and gld mice produced less apoptosis when coincubated with C.B10-H2(b)/LilMcd (C.B10) BM cells in vitro. This functional difference was confirmed by infusing lpr, gld, and B6 LN cells into sublethally irradiated CB10 mice. All donor LN cells showed significant T cell expansion and activation, but only B6 LN cells caused severe BM destruction. Mice infused with gld LN cells developed mild to moderate BM failure despite receiving FasL-deficient effectors, thus suggesting the existence of alternative pathways or incomplete penetrance of the mutation. Paradoxically, mice that received Fas-deficient lpr LN cells also had reduced BM failure, likely due to down-regulation of proapoptotic genes, an effect that can be overcome by higher doses of lpr LN cells. Our model demonstrates that abnormal Fas or FasL expression interferes with the development of pancytopenia and marrow hypoplasia, validating a major role for the Fas/FasL cytotoxic pathway in immune-mediated BM failure, although disruption of this pathway does not completely abolish marrow destruction.

Indexed as

AnimalsApoptosisBone Marrow DiseasesClone CellsDisease Models, AnimalFas Ligand Proteinfas ReceptorGene Expression RegulationLymphocyte SubsetsLymphoproliferative DisordersMiceMice, CongenicMice, Inbred C57BLMice, Inbred MRL lprMice, Mutant StrainsFas Ligand Proteinfas Receptor

Identifiers

PMID19265119
PMCPMC3513944
OpenAlexW2107919026

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.