Evidence map›Paper›PMID 26449606›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

T Cell CX3CR1 Mediates Excess Atherosclerotic Inflammation in Renal Impairment.

Lei Dong, Johannes Nordlohne, Shuwang Ge, Barbara Hertel, Anette Melk, Song Rong, Hermann Haller, Sibylle von Vietinghoff

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Peritoneal Dialysis Aggravates and Accelerates Atherosclerosis in UremicJournal of the American Heart Association · 2024
    Article
  5. Article
  6. CXInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  7. Article
  8. Immunosenescence: an unexplored role in glomerulonephritis.Clinical & translational immunology · 2022
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

8 authors at 2 institutions in 2 countries.

Lei DongDivision of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany; Department of Nephrology, Tongji Hospital, Huazhong University of Science and Technology, China; and.
Johannes NordlohneDivision of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany;
Shuwang GeDivision of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany; Department of Nephrology, Tongji Hospital, Huazhong University of Science and Technology, China; and.
Barbara HertelDivision of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany;
Anette MelkDivision of Pediatrics, Hannover Medical School, Hannover, Germany.
Song RongDivision of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany;
Hermann HallerDivision of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany;
Sibylle von VietinghoffDivision of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany; vonVietinghoff.Sibylle@mh-hannover.de.
Medizinische Hochschule Hannover · DEHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reduced kidney function increases the risk for atherosclerosis and cardiovascular death. Leukocytes in the arterial wall contribute to atherosclerotic plaque formation. We investigated the role of fractalkine receptor CX3CR1 in atherosclerotic inflammation in renal impairment. Apoe(-/-) (apolipoprotein E) CX3CR1(-/-) mice with renal impairment were protected from increased aortic atherosclerotic lesion size and macrophage accumulation. Deficiency of CX3CR1 in bone marrow, only, attenuated atherosclerosis in renal impairment in an independent atherosclerosis model of LDL receptor-deficient (LDLr(-/-)) mice as well. Analysis of inflammatory leukocytes in atherosclerotic mixed bone-marrow chimeric mice (50% wild-type/50% CX3CR1(-/-) bone marrow into LDLr(-/-) mice) showed that CX3CR1 cell intrinsically promoted aortic T cell accumulation much more than CD11b(+)CD11c(+) myeloid cell accumulation and increased IL-17-producing T cell counts. In vitro, fewer TH17 cells were obtained from CX3CR1(-/-) splenocytes than from wild-type splenocytes after polarization with IL-6, IL-23, and TGFβ Polarization of TH17 or TREG cells, or stimulation of splenocytes with TGFβ alone, increased T cell CX3CR1 reporter gene expression. Furthermore, TGFβ induced CX3CR1 mRNA expression in wild-type cells in a dose- and time-dependent manner. In atherosclerotic LDLr(-/-) mice, CX3CR1(+/-) T cells upregulated CX3CR1 and IL-17A production in renal impairment, whereas CX3CR1(-/-) T cells did not. Transfer of CX3CR1(+/-) but not Il17a(-/-) T cells into LDLr(-/-)CX3CR1(-/-) mice increased aortic lesion size and aortic CD11b(+)CD11c(+) myeloid cell accumulation in renal impairment. In summary, T cell CX3CR1 expression can be induced by TGFβ and is instrumental in enhanced atherosclerosis in renal impairment.

Indexed as

AnimalsAtherosclerosisCells, CulturedCX3C Chemokine Receptor 1FemaleInflammationMaleMiceReceptors, ChemokineRenal InsufficiencyCX3C Chemokine Receptor 1Cx3cr1 protein, mouseReceptors, Chemokinearteriosclerosischemokine receptorlymphocytes

Identifiers

PMID26449606
PMCPMC4884117
OpenAlexW2183555200

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.