Evidence map›Paper›PMID 22177564›Full record

ArticleCell host & microbe2011

The β-glucan receptor Dectin-1 activates the integrin Mac-1 in neutrophils via Vav protein signaling to promote Candida albicans clearance.

Xun Li, Ahmad Utomo, Xavier Cullere, Myunghwan Mark Choi, Danny A Milner, Deepak Venkatesh, Seok-Hyun Yun, Tanya N Mayadas

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

89 citing papers in PubMed, 147 citations in OpenAlex.

  1. Trial
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  6. Loss of Fgr41 inInfection and immunity · 2026
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  9. Microorganisms · 2025
    Review
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  11. Review
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  13. Review
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  15. Article
  16. Article
  17. Article
  18. Article
  19. Targeting Neutrophil βBiomolecules · 2023
    Review
  20. Dual wave of neutrophil recruitment determines the outcome ofFrontiers in cellular and infection microbiology · 2023
    Article

29 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

8 authors at 2 institutions in 1 country.

Xun LiCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Ahmad Utomo
Xavier Cullere
Myunghwan Mark Choi
Danny A Milner
Deepak Venkatesh
Seok-Hyun Yun
Tanya N Mayadas
Harvard University · USBrigham and Women's Hospital · US

Funding

Regulators of Immune Complex Mediated Neutrophil Recruitment and Tissue InjuryR01HL065095 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N · 1999 to 2025
$11.9M
MAC-1(CR3) IN IMMUNE-MEDIATED NEUTROPHIL CYTOTOXICITYR01AR050800 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N · 2003 to 2013
$3.3M
DOCK4 regulation of small GTPases in vascular permeabilityK01AR054984 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI CULLERE, FRANCISCO · 2007 to 2011
$647k
NHLBI NIH HHS HL065095NHLBI NIH HHS R01 HL065095NIAMS NIH HHS K01 AR054984NIAMS NIH HHS R01 AR050800
6 · The paper itself

Abstract

Resistance to fungal infections is attributed to engagement of host pattern-recognition receptors, notably the β-glucan receptor Dectin-1 and the integrin Mac-1, which induce phagocytosis and antifungal immunity. However, the mechanisms by which these receptors coordinate fungal clearance are unknown. We show that upon ligand binding, Dectin-1 activates Mac-1 to also recognize fungal components, and this stepwise process is critical for neutrophil cytotoxic responses. Both Mac-1 activation and Dectin-1- and Mac-1-induced neutrophil effector functions require Vav1 and Vav3, exchange factors for RhoGTPases. Mac-1- or Vav1,3-deficient mice have increased susceptibility to systemic candidiasis that is not due to impaired neutrophil recruitment but defective intracellular killing of C. albicans yeast forms, and Mac-1 or Vav1,3 reconstitution in hematopoietic cells restores resistance. Our results demonstrate that antifungal immunity depends on Dectin-1-induced activation of Mac-1 functions that is coordinated by Vav proteins, a pathway that may localize cytotoxic responses of circulating neutrophils to infected tissues.

Indexed as

AnimalsCandida albicansCandidiasisDectin-1FemaleHumansLectins, C-TypeMacrophage-1 AntigenMaleMiceMice, Inbred C57BLMice, KnockoutNeutrophilsPhagocytosisProto-Oncogene Proteins c-vavReceptors, Immunologicbeta-glucan receptorDectin-1Lectins, C-TypeMacrophage-1 AntigenProto-Oncogene Proteins c-vavReceptors, ImmunologicVav1 protein, mouseVav3 protein, mouse

Identifiers

PMID22177564
PMCPMC3244687
OpenAlexW2150097442

What OpenQuestion holds

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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.