Evidence map›Paper›PMID 27315778›Full record

ArticleThe American journal of pathology2016

The Role of Integrins αMβ2 (Mac-1, CD11b/CD18) and αDβ2 (CD11d/CD18) in Macrophage Fusion.

Nataly P Podolnikova, Yevgeniya S Kushchayeva, YiFei Wu, James Faust, Tatiana P Ugarova

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. TARGETING THE CAPSULE OFbioRxiv : the preprint server for biology · 2026
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  13. Innate Pulmonary Phagocytes and Their Interactions with PathogenicJournal of fungi (Basel, Switzerland) · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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 1 institution in 1 country.

Nataly P PodolnikovaCenter for Metabolic and Vascular Biology, School of Life Sciences, Arizona State University, Tempe, Arizona.
Yevgeniya S KushchayevaCenter for Metabolic and Vascular Biology, School of Life Sciences, Arizona State University, Tempe, Arizona.
YiFei WuCenter for Metabolic and Vascular Biology, School of Life Sciences, Arizona State University, Tempe, Arizona.
James FaustCenter for Metabolic and Vascular Biology, School of Life Sciences, Arizona State University, Tempe, Arizona.
Tatiana P UgarovaCenter for Metabolic and Vascular Biology, School of Life Sciences, Arizona State University, Tempe, Arizona. Electronic address: tatiana.ugarova@asu.edu.
Arizona State University · US

Funding

The role of beta 2 integrins in macrophage fusionR01HL063199 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI Tatiana P Ugarova · 1999 to 2026
$8.6M
NHLBI NIH HHS R01 HL063199
6 · The paper itself

Abstract

The subfamily of β2 integrins is implicated in macrophage fusion, a hallmark of chronic inflammation. Among β2 family members, integrin Mac-1 (αMβ2, CD11b/CD18) is abundantly expressed on monocyte/macrophages and mediates critical adhesive reactions of these cells. However, the role of Mac-1 in macrophage fusion leading to the formation of multinucleated giant cells remains unclear. Moreover, the role of integrin αDβ2 (CD11d/CD18), a receptor with recognition specificity overlapping that of Mac-1, is unknown. We found that multinucleated giant cells are formed in the inflamed mouse peritoneum during the resolution phase of inflammation, and their numbers were approximately twofold higher in wild-type mice than in Mac-1(-/-) mice. Analyses of isolated inflammatory peritoneal macrophages showed that IL-4-induced fusion of Mac-1-deficient cells was strongly reduced compared with wild-type counterparts. The examination of adhesive reactions known to be required for fusion showed that spreading, but not adhesion and migration, was reduced in Mac-1-deficient macrophages. Fusion of αDβ2-deficient macrophages was also significantly decreased, albeit to a smaller degree. Deficiency of intercellular adhesion molecule 1, a counter-receptor for Mac-1 and αDβ2, did not alter the fusion rate. The results indicate that both Mac-1 and αDβ2 support macrophage fusion with Mac-1 playing a dominant role and suggest that Mac-1 may mediate cell-cell interactions with a previously unrecognized counter-receptor(s).

Indexed as

AnimalsCD11 AntigensCell FusionDisease Models, AnimalFlow CytometryFluorescent Antibody TechniqueGiant CellsInflammationIntegrin alpha ChainsMacrophage-1 AntigenMacrophagesMiceMice, Inbred C57BLMice, KnockoutPeritonitisCD11 AntigensIntegrin alpha Chainsintegrin alphaD, mouseMacrophage-1 Antigen

Identifiers

PMID27315778
PMCPMC4973655
OpenAlexW2425613501

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.