Evidence map›Paper›PMID 22884314›Full record

ArticleImmunity2012

Galectin-1 deactivates classically activated microglia and protects from inflammation-induced neurodegeneration.

Sarah C Starossom, Ivan D Mascanfroni, Jaime Imitola, Li Cao, Khadir Raddassi, Silvia F Hernandez, Ribal Bassil, Diego O Croci, Juan P Cerliani, Delphine Delacour and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed, 2 pooled it
10.8field-weighted citation impact, top 1% 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

198 citing papers in PubMed, 2 syntheses or guidelines pooled it, 356 citations in OpenAlex.

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  13. Stromal-Like Cells and Retinal Pigment Epithelium Modulate Choroidal Sprouting Through Galectin-1-Dependent and Independent Pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  14. Review
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138 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 5 countries.

Sarah C StarossomCenter for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Ivan D Mascanfroni
Jaime Imitola
Li Cao
Khadir Raddassi
Silvia F Hernandez
Ribal Bassil
Diego O Croci
Juan P Cerliani
Delphine Delacour
Yue Wang
Wassim Elyaman
Samia J Khoury
Gabriel A Rabinovich
Brigham and Women's Hospital · USConsejo Nacional de Investigaciones Científicas y Técnicas · ARCentre National de la Recherche Scientifique · FR

Funding

Immune Regulation of Neural Stem Cell Program In EAER01AI043496 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KHOURY, SAMIA J. · 1999 to 2015
$3.9M
Impact of IFN-gamma on Neural Stem Cell Repair Potential in EAER01AI071448 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KHOURY, SAMIA J. · 2007 to 2010
$1.4M
Role and Mechanism of PDI-PDL Pathway in EAER01AI058680 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KHOURY, SAMIA J. · 2004 to 2007
$1.3M
Role and mechanism of negative costimulatory pathways in EAER56AI058680 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI KHOURY, SAMIA J. · 2009 to 2010
$804k
NIAID NIH HHS AI058680NIAID NIH HHS AI071448NIAID NIH HHS R01 AI043496NIAID NIH HHS R01 AI058680NIAID NIH HHS R01 AI071448NIAID NIH HHS R56 AI058680
6 · The paper itself

Abstract

Inflammation-mediated neurodegeneration occurs in the acute and the chronic phases of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Classically activated (M1) microglia are key players mediating this process. Here, we identified Galectin-1 (Gal1), an endogenous glycan-binding protein, as a pivotal regulator of M1 microglial activation that targets the activation of p38MAPK-, CREB-, and NF-κB-dependent signaling pathways and hierarchically suppresses downstream proinflammatory mediators, such as iNOS, TNF, and CCL2. Gal1 bound to core 2 O-glycans on CD45, favoring retention of this glycoprotein on the microglial cell surface and augmenting its phosphatase activity and inhibitory function. Gal1 was highly expressed in the acute phase of EAE, and its targeted deletion resulted in pronounced inflammation-induced neurodegeneration. Adoptive transfer of Gal1-secreting astrocytes or administration of recombinant Gal1 suppressed EAE through mechanisms involving microglial deactivation. Thus, Gal1-glycan interactions are essential in tempering microglial activation, brain inflammation, and neurodegeneration, with critical therapeutic implications for MS.

Indexed as

AnimalsAstrocytesCentral Nervous SystemChemokine CCL2Cyclic AMP Response Element-Binding ProteinEncephalomyelitis, Autoimmune, ExperimentalFemaleGalectin 1HumansInterleukin-6Leukocyte Common AntigensMiceMice, Inbred C57BLMice, KnockoutMicrogliaMultiple SclerosisChemokine CCL2Cyclic AMP Response Element-Binding ProteinGalectin 1Interleukin-6Leukocyte Common AntigensNF-kappa BNitric Oxide Synthase Type IIp38 Mitogen-Activated Protein KinasesPolysaccharidesTumor Necrosis Factor-alpha

Identifiers

PMID22884314
PMCPMC3428471
OpenAlexW2080432978

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.