Evidence map›Paper›PMID 21335485›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

A New Zealand Black-derived locus suppresses chronic graft-versus-host disease and autoantibody production through nonlymphoid bone marrow-derived cells.

Zhiwei Xu, Anusha Vallurupalli, Christopher Fuhrman, David Ostrov, Laurence Morel

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. 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
1.7field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Contribution of Dendritic Cell Subsets to T Cell-Dependent Responses in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  2. Article
  3. Article
  4. Article
  5. T-betArthritis research & therapy · 2017
    Article
  6. An update on lupus animal models.Current opinion in rheumatology · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Autoimmunity in 2011.Clinical reviews in allergy & immunology · 2012
    Review
  13. Article
  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

5 authors at 1 institution in 1 country.

Zhiwei XuDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610, USA.
Anusha Vallurupalli
Christopher Fuhrman
David Ostrov
Laurence Morel
University of Florida · US

Funding

Genetic dissection of Sle2 contribution to SLE pathogenesisR01AI068965 · NIAID · UNIVERSITY OF FLORIDA · PI MOREL, LAURENCE · 2006 to 2010
$1.7M
Genetic and Functional Analysis of IL-2 Deficiency in Lupus-Prone MiceK01AR056725 · NIAMS · UNIVERSITY OF FLORIDA · PI XU, ZHIWEI · 2009 to 2013
$531k
NIAID NIH HHS R01 AI068965NIAMS NIH HHS K01 AR056725NIAMS NIH HHS K01AR056725
6 · The paper itself

Abstract

The development of lupus pathogenesis results from the integration of susceptibility and resistance genes. We have used a chronic graft-versus-host disease (cGVHD) model to characterize a suppressive locus at the telomeric end of the NZM2410-derived Sle2 susceptibility locus, which we named Sle2c2. cGVHD is induced normally in Sle2c2-expressing mice, but it is not sustained. The analysis of mixed bone marrow chimeras revealed that cGVHD resistance was eliminated by non-B non-T hematopoietic cells expressing the B6 allele, suggesting that resistance is mediated by this same cell type. Furthermore, Sle2c2 expression was associated with an increased number and activation of the CD11b(+) GR-1(+) subset of granulocytes before and in the early stage of cGVHD induction. We have mapped the Sle2c2 critical interval to a 6-Mb region that contains the Cfs3r gene, which encodes for the G-CSFR, and its NZM2410 allele carries a nonsynonymous mutation. The G-CSFR-G-CSF pathway has been previously implicated in the regulation of GVHD, and our functional data on Sle2c2 suppression suggest a novel regulation of T cell-induced systemic autoimmunity through myeloid-derived suppressor cells. The validation of Csf3r as the causative gene for Sle2c2 and the further characterization of the Sle2c2 MDSCs promise to unveil new mechanisms by which lupus pathogenesis is regulated.

Indexed as

Genetic Predisposition to DiseaseAnimalsAntibodies, AntinuclearBone Marrow CellsChronic DiseaseDisease Models, AnimalGenes, SuppressorGenetic LociGraft vs Host DiseaseImmune ToleranceLupus Erythematosus, SystemicMiceMice, Inbred C57BLMice, Inbred NZBMice, KnockoutMyeloid CellsAntibodies, Antinuclear

Identifiers

PMID21335485
PMCPMC3131784
OpenAlexW1909042374

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.