CoChat
Sign Up
Cited by 122Neuroinflammation and Neurodegeneration MechanismsMultiple Sclerosis Research StudiesTGF-β signaling in diseases

The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.

TGFβ directs gene expression of activated microglia to an anti‐inflammatory phenotype strongly focusing on chemokine genes and cell migratory genes

Open access
Paglinawan, Rey, Malipiero, Ursula, Schlapbach, Ralph, Frei, Karl, Reith, Walter, Fontana, Adriano·2003·Glia
DOI 10.1002/glia.10286
Open this paper in CoChat — free account

Abstract

In experimental autoimmune encephalomyelitis, the acute phase of the disease is produced by T‐helper lymphocyte type 1 (T H 1), which produces mainly TNFα and IFNγ. Recovery from the disease is mediated by T‐helper lymphocyte types 2 and 3 (T H 2/T H 3), which, among other cytokines, produce transforming growth factor β (TGFβ). To address the influence of TGFβ on T H 1‐induced gene expression, microarray technology was used on murine primary microglial cells stimulated with IFNγ and TNFα in the absence or presence of TGFβ. The resulting data from an investigation of up to 5,500 genes provided the notion that TGFβ prevents the induction of a proinflammatory gene program within microglia exposed to a T H 1 milieu. T H 1 cytokines upregulated 175 genes comprising cytokine, chemokine, and genes involved in host response to infection and the TNFα/IFNγ intracellular signaling pathway. It is observed that TGFβ inhibits expression of 25% of the TNFα/IFNγ‐induced genes and a further 66 TNFα/IFNγ‐independent genes. The focus of TGFβ inhibition is observed to be directed in genes involved in chemotaxis (IL‐15, CXCL1, CXCL2, CCL3, CCL4, CCL5, CCL9), chemokine receptors (CCR5, CCR9), LIF receptor, and FPR2, and on genes mediating cell migration (MMP9, MMP13, MacMARCKS, endothelin receptor B, Ena/VASP, Gas7), apoptosis (FAS, TNF, TNF receptor, caspase‐1 and ‐11), and host response to infection (toll‐like receptor 6, Mx‐1, and MARCO). Taken collectively, the data strongly suggest that one of the main effects of TGFβ is to impair cell entry into the CNS and to hinder migration of microglia in the CNS parenchyma. © 2003 Wiley‐Liss, Inc.

Overview

Integrity signals

Registry

Crossref · 10.1002/glia.10286

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 43 references

Cited by

Sorted by citations

Items 101–121 of 121

Related

See all

Metadata

Authors
Paglinawan, R., Malipiero, U., Schlapbach, R., Frei, K., Reith, W., & Fontana, A.
Affiliations
  • University Hospital Zurich (CH)
  • Functional Genomics Center Zurich (CH)
  • University of Geneva (CH)
Corresponding author
Fontana, Adriano
ORCID
Schlapbach, Ralph
Venue
Glia
Publisher
Wiley
Published
2003-08
Volume
44
Issue
3
Pages
219-231
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
DOI
10.1002/glia.10286
OpenAlex
W2022786490
Cited by
122
References
43
Citations by year
2026: 2 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 2 · 2021: 6 · 2020: 3 · 2019: 6 · 2018: 6 · 2017: 5 · 2016: 9 · 2015: 7 · 2014: 4 · 2013: 8 · 2012: 4
FWCI
3.73
Type
journal article
Language
en
Open access
Licence
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
TGF-beta, microglia, experimental autoimmune encephalomyelitis, Th1 cytokines, interferon-gamma, TNF-α, anti-inflammatory phenotype, chemokine genes, cell migration, chemotaxis, chemokine receptors, apoptosis, host response to infection, gene expression profiling
MeSH terms
Animals, Cell Movement, Encephalomyelitis, Autoimmune, Experimental, Gene Expression Regulation, Phenotype, Specific Pathogen-Free Organisms, Transforming Growth Factor beta, Apoptosis, Microglia, Chemokines, Oligonucleotide Array Sequence Analysis, Mice, Transforming Growth Factor beta2

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review