Evidence map›Paper›PMID 22438246›Full record

ArticleBlood2012

Galectin-9 binding to Tim-3 renders activated human CD4+ T cells less susceptible to HIV-1 infection.

Shokrollah Elahi, Toshiro Niki, Mitsuomi Hirashima, Helen Horton

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. TIM-3, a potential target for sepsis therapy.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026
    Review
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  12. Observational
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  20. Immunological responses in SARS-CoV-2 and HIV co-infection versus SARS-CoV-2 mono-infection: case report of the interplay between SARS-CoV-2 and HIV.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Article

25 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Shokrollah ElahiViral Vaccine Program, Seattle Biomedical Research Institute (Seattle Biomed), 307 Westlake Ave N, Seattle, WA 98109, USA.
Toshiro Niki
Mitsuomi Hirashima
Helen Horton
Center for Infectious Disease Research · USKagawa University · JP

Funding

University of Washington/Fred Hutch Center for AIDS ResearchP30AI027757 · NIAID · UNIVERSITY OF WASHINGTON · PI Kenneth Sherr · 1988 to 2026
$104.9M
ZIPRASIDONE IN NORMAL HEPATIC FUNCTION SUBJECTS &IN HEPATIC DYSFUCTIN SUBJECTSM01RR000037 · NCRR · UNIVERSITY OF WASHINGTON · PI MCDONALD, RUTH C · 1985 to 2007
$33.8M
Activation-induced Non-responsiveness causes HIV Prog.R01AI065328 · NIAID · SEATTLE BIOMEDICAL RESEARCH INSTITUTE · PI HORTON, HELEN · 2005 to 2009
$1.6M
Tregs Differentially Suppress HIV-specific CD8+ T CellsR21AI089373 · NIAID · SEATTLE BIOMEDICAL RESEARCH INSTITUTE · PI HORTON, HELEN · 2010 to 2011
$538k
NCRR NIH HHS M01 RR000037NCRR NIH HHS M01-RR-00037NIAID NIH HHS P30 AI027757NIAID NIH HHS P30 AI127757NIAID NIH HHS R01 AI065328NIAID NIH HHS R01 AI65328NIAID NIH HHS R21 AI089373
6 · The paper itself

Abstract

Galectin-9 (Gal-9) is a tandem repeat-type member of the galectin family and is a ligand for T-cell immunoglobulin mucin domain 3 (Tim-3), a type-I glycoprotein that is persistently expressed on dysfunctional T cells during chronic infection. Studies in autoimmune diseases and chronic viral infections show that Tim-3 is a regulatory molecule that inhibits Th1 type immune responses. Here we show that soluble Gal-9 interacts with Tim-3 expressed on the surface of activated CD4(+) T cells and renders them less susceptible to HIV-1 infection and replication. The Gal-9/Tim-3 interaction on activated CD4(+) T cells, leads to down-regulation of HIV-1 coreceptors and up-regulation of the cyclin-dependent kinase inhibitor p21 (also known as cip-1 and waf-1). We suggest that higher expression of Tim-3 during chronic infection has evolved to limit persistent immune activation and associated tissue damage. These data demonstrate a novel mechanism for Gal-9/Tim-3 interactions to induce resistance of activated CD4(+) T cells to HIV-1 infection and suggest that Gal-9 may play a role in HIV-1 pathogenesis and could be used as a novel microbicide to prevent HIV-1 infection.

Indexed as

ApoptosisCD4-Positive T-LymphocytesCells, CulturedCyclin-Dependent Kinase Inhibitor p21GalectinsGene Expression RegulationGenes, p53Hepatitis A Virus Cellular Receptor 2HIV-1HIV InfectionsHumansIntegrinsLymphocyte ActivationMembrane ProteinsProtein BindingProtein Interaction MappingCDKN1A protein, humanCXCR4 protein, humanCXCR5 protein, humanCyclin-Dependent Kinase Inhibitor p21GalectinsHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2integrin alpha4beta7IntegrinsLGALS9 protein, humanMembrane ProteinsReceptors, CXCR4Receptors, CXCR5RNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22438246
PMCPMC3359739
OpenAlexW2076803727

What OpenQuestion holds

Textmetadata
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.