Evidence map›Paper›PMID 25792447›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Reduced Atherosclerosis in apoE-inhibitory FcγRIIb-Deficient Mice Is Associated With Increased Anti-Inflammatory Responses by T Cells and Macrophages.

Hang Pong Ng, Xinmei Zhu, Erin Y Harmon, Michelle R Lennartz, Shanmugam Nagarajan

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Atherosclerosis antigens as targets for immunotherapy.Nature cardiovascular research · 2023
    Review
  4. Fcα Receptor Type I and Its Association with Atherosclerosis Development.Juntendo Iji zasshi = Juntendo medical journal · 2023
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. FcγRIIb on CD11cAtherosclerosis · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Interaction between allergic asthma and atherosclerosis.Translational research : the journal of laboratory and clinical medicine · 2016
    Review
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 2 institutions in 1 country.

Hang Pong NgFrom the Department of Pathology, Vascular Medicine Institute, University of Pittsburgh, PA (H.P.N., X.Z., S.N.); Department of Microbiology and Immunology (H.P.N., S.N.), University of Arkansas for Medical Sciences, Little Rock; and Center for Cell Biology and Cancer Research, Albany Medical College, NY (E.Y.H., M.R.L.).
Xinmei ZhuFrom the Department of Pathology, Vascular Medicine Institute, University of Pittsburgh, PA (H.P.N., X.Z., S.N.); Department of Microbiology and Immunology (H.P.N., S.N.), University of Arkansas for Medical Sciences, Little Rock; and Center for Cell Biology and Cancer Research, Albany Medical College, NY (E.Y.H., M.R.L.).
Erin Y HarmonFrom the Department of Pathology, Vascular Medicine Institute, University of Pittsburgh, PA (H.P.N., X.Z., S.N.); Department of Microbiology and Immunology (H.P.N., S.N.), University of Arkansas for Medical Sciences, Little Rock; and Center for Cell Biology and Cancer Research, Albany Medical College, NY (E.Y.H., M.R.L.).
Michelle R LennartzFrom the Department of Pathology, Vascular Medicine Institute, University of Pittsburgh, PA (H.P.N., X.Z., S.N.); Department of Microbiology and Immunology (H.P.N., S.N.), University of Arkansas for Medical Sciences, Little Rock; and Center for Cell Biology and Cancer Research, Albany Medical College, NY (E.Y.H., M.R.L.).
Shanmugam NagarajanFrom the Department of Pathology, Vascular Medicine Institute, University of Pittsburgh, PA (H.P.N., X.Z., S.N.); Department of Microbiology and Immunology (H.P.N., S.N.), University of Arkansas for Medical Sciences, Little Rock; and Center for Cell Biology and Cancer Research, Albany Medical College, NY (E.Y.H., M.R.L.). Nagarajans@upmc.edu.
University of Arkansas for Medical Sciences · USUniversity of Pittsburgh · US

Funding

Role of Fc gamma receptors in atherosclerosisR01HL086674 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NAGARAJAN, SHANMUGAM · 2008 to 2012
$1.8M
Role of Fc Receptor in atherosclerotic plaque progressionR21HL089730 · NHLBI · ALBANY MEDICAL COLLEGE · PI LENNARTZ, MICHELLE R · 2008 to 2009
$412k
Role of Macrophage Activation in Carotid Plaque InstabilityR21HL095971 · NHLBI · ALBANY MEDICAL COLLEGE · PI LENNARTZ, MICHELLE R · 2009 to 2010
$407k
NHLBI NIH HHS HL089730NHLBI NIH HHS HL095971NHLBI NIH HHS R01 HL086674NHLBI NIH HHS R01HL086674NHLBI NIH HHS R21 HL089730NHLBI NIH HHS R21 HL095971NIGMS NIH HHS GM09032507
6 · The paper itself

Abstract

objectiveFcγ receptors (FcγRs) are classified as activating (FcγRI, III, and IV) and inhibitory (FcγRII) receptors. We have reported that deletion of activating FcγRs in apolipoprotein E (apoE) single knockout mice attenuated atherosclerosis. In this report, we investigated the hypothesis that deficiency of inhibitory FcγRIIb exacerbates atherosclerosis. APPROACH AND

resultsApoE-FcγRIIb double knockout mice, congenic to the C57BL/6 (apoE-FcγRIIbB6 (-/-)), were generated and atherosclerotic lesions were assessed. In contrary to our hypothesis, when compared with apoE single knockout mice, arterial lesions were significantly decreased in apoE-FcγRIIbB6 (-/-) male and female mice fed chow or high-fat diets. Chimeric mice generated by transplanting apoE-FcγRIIbB6 (-/-) marrow into apoE single knockout mice also developed reduced lesions. CD4(+) T cells from apoE-FcγRIIbB6 (-/-) mice produced higher levels of interleukin-10 and transforming growth factor-β than their apoE single knockout counterparts. As our findings conflict with a previous report using apoE-FcγRIIb129/B6 (-/-) mice on a mixed genetic background, we investigated whether strain differences contributed to the anti-inflammatory response. Macrophages from FcγRIIb129/B6 (-/-) mice on a mixed genetic background produced more interleukin-1β and MCP-1 (monocyte chemoattractant protein-1) in response to immune complexes, whereas congenic FcγRIIbB6 (-/-) mice generated more interleukin-10 and significantly less interleukin-1β. Interestingly, the expression of lupus-associated slam genes, located in proximity to fcgr2b in mouse chromosome 1, is upregulated only in mixed FcγRIIb129/B6 (-/-) mice.

conclusionsOur findings demonstrate a detrimental role for FcγRIIb signaling in atherosclerosis and the contribution of anti-inflammatory cytokine responses in the attenuated lesions observed in apoE-FcγRIIbB6 (-/-) mice. As 129/sv genome-derived lupus-associated genes have been implicated in lupus phenotype in FcγRIIb129/B6 (-/-) mice, our findings suggest possible epistatic mechanism contributing to the decreased lesions.

Indexed as

AnimalsApolipoproteins EAtherosclerosisCD4 AntigensCytokinesDisease Models, AnimalFemaleInflammation MediatorsMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutRandom AllocationReceptors, IgGSensitivity and SpecificityApolipoproteins ECD4 AntigensCytokinesInflammation MediatorsReceptors, IgGantibody productionatherosclerosisautoimmune diseasesFc gamma receptorsoxidized low-density lipoprotein

Identifiers

PMID25792447
PMCPMC4409543
OpenAlexW1979002372

What OpenQuestion holds

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LicenceTDM
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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.