Evidence map›Paper›PMID 22595426›Full record

ArticleMolecular genetics and metabolism2012

Immunological cell type characterization and Th1-Th17 cytokine production in a mouse model of Gaucher disease.

Manoj Kumar Pandey, Reena Rani, Wujuan Zhang, Kenneth Setchell, Gregory A Grabowski

Open access · greenAbstract read
In one paragraph

Article in Molecular genetics and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Sphingolipids in Gaucher disease: a systematic review.Orphanet journal of rare diseases · 2025
    Pooled it
  2. Central Roles of Glucosylceramide in Driving Cancer Pathogenesis.International journal of molecular sciences · 2025
    Review
  3. Deciphering metabolic shifts in Gaucher disease type 1: a multi-omics study.Journal of molecular medicine (Berlin, Germany) · 2025
    Article
  4. Old disease-New reflections: Gaucher, immunity, and inflammation.Journal of cellular and molecular medicine · 2024
    Review
  5. Article
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  8. Review
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  10. Article
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  13. Review
  14. Hypoxia-induced Pulmonary Hypertension in Different Mouse Strains: Relation to Transcriptome.American journal of respiratory cell and molecular biology · 2019
    Article
  15. Dual Expression of theFrontiers in microbiology · 2017
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Manoj Kumar PandeyDivision of Human Genetics, Cincinnati Children's Hospital Medical Center, and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45229‐3039, USA.
Reena Rani
Wujuan Zhang
Kenneth Setchell
Gregory A Grabowski
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · US

Funding

STUDIES OF GAUCHER DISEASE: A PROTOTYPE LIPIDOSISR01DK036729 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF CUNY · PI GRABOWSKI, GREGORY A. · 1986 to 2011
$4.5M
NIDDK NIH HHS DK36749NIDDK NIH HHS R01 DK036729
6 · The paper itself

Abstract

Gaucher disease is a lysosomal storage disease resulting from insufficient acid β-glucosidase (glucocerebrosidase, GCase, EC 4.2.1.25) activity and the resultant accumulation of glucosylceramide. Macrophage (Mϕ) lineage cells are thought to be the major disease effectors because of their secretion of numerous cytokines and chemokines that influence other poorly defined immunological cell populations. Increases in several such populations were identified in a Gba1 mouse model (D409V/null; 9V/null) of Gaucher disease including antigen presenting cells (APCs), i.e., Mϕ, dendritic cells (DCs), neutrophils (PMNs), and CD4(+) T cells. FACS analyses showed increases in these cell types in 9V/null liver, spleen lung, and bone marrow. T-cells or APCs enhanced activations were evident by positivity of CD40L, CD69, as well as CD40, CD80, CD86, and MHCII on the respective cells. Mϕ, and, unexpectedly, DCs, PMNs, and T cells, from 9V/null mice showed excess glucosylceramides as potential bases for activation of APCs and T cells to induce Th1 (IFNγ, IL12, TNFα,) and Th17 (IL17A/F) cytokine production. These data imply that excess glucosylceramides in these cells are pivotal for activation of APCs and T cell induction of Th1 and Th17 responses and PMN recruitment in multiple organs of this model of Gaucher disease.

Indexed as

AnimalsAntigen-Presenting CellsCD28 AntigensCD3 ComplexCytokinesDendritic CellsDisease Models, AnimalGaucher DiseaseMacrophagesMiceMice, Inbred StrainsSpleenTh17 CellsTh1 CellsCD28 AntigensCD3 ComplexCytokines

Identifiers

PMID22595426
PMCPMC3382074
OpenAlexW2078235658

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.