Evidence map›Paper›PMID 21677140›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Circulating activated and effector memory T cells are associated with calcification and clonal expansions in bicuspid and tricuspid valves of calcific aortic stenosis.

Robert Winchester, Margrit Wiesendanger, Will O'Brien, Hui-Zhu Zhang, Mathew S Maurer, Linda D Gillam, Allan Schwartz, Charles Marboe, Allan S Stewart

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Age Differences in Aortic Stenosis.Reviews in cardiovascular medicine · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Calcific Aortic Valve Stenosis with Aging and Current Development in its Pathophysiology.The International journal of angiology : official publication of the International College of Angiology, Inc · 2022
    Article
  10. Article
  11. Review
  12. Lipoprotein(a), a Lethal Player in Calcific Aortic Valve Disease.Frontiers in cell and developmental biology · 2022
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Adaptive immune cells in calcific aortic valve disease.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  18. Article
  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

9 authors at 1 institution in 1 country.

Robert WinchesterDivision of Rheumatology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA. rjw8@columbia.edu
Margrit Wiesendanger
Will O'Brien
Hui-Zhu Zhang
Mathew S Maurer
Linda D Gillam
Allan Schwartz
Charles Marboe
Allan S Stewart
Columbia University · US

Funding

Immunopathogenic features in calcific aortic stenosisR01HL084599 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI WINCHESTER, ROBERT J · 2006 to 2009
$1.5M
NHLBI NIH HHS R01 HL084599
6 · The paper itself

Abstract

We sought to delineate further the immunological significance of T lymphocytes infiltrating the valve leaflets in calcific aortic stenosis (CAS) and determine whether there were associated alterations in circulating T cells. Using clonotypic TCR β-chain length and sequence analysis we confirmed that the repertoire of tricuspid CAS valves contains numerous expanded T cell clones with varying degrees of additional polyclonality, which was greatest in cases with severe calcification. We now report a similar proportion of clonal expansions in the much younger bicuspid valve CAS cases. Peripheral blood flow cytometry revealed elevations in HLA-DR(+) activated CD8 cells and in the CD8(+)CD28(null)CD57(+) memory-effector subset that were significantly greater in both bicuspid and tricuspid CAS cases with more severe valve calcification. Lesser increases of CD4(+)CD28(null) T cells were identified, principally in cases with concurrent atherosclerotic disease. Upon immunostaining the CD8 T cells in all valves were mainly CD28(null), and CD8 T cell percentages were greatest in valves with oligoclonal repertoires. T cell clones identified by their clonotypic sequence as expanded in the valve were also found expanded in the circulating blood CD28(null)CD8(+) T cells and to a lesser degree in the CD8(+)CD28(+) subset, directly supporting the relationship between immunologic events in the blood and the valve. The results suggest that an ongoing systemic adaptive immune response is occurring in cases with bicuspid and tricuspid CAS, involving circulating CD8 T cell activation, clonal expansion, and differentiation to a memory-effector phenotype, with trafficking of T cells in expanded clones between blood and the valve.

Indexed as

Immunologic MemoryAdultAgedAged, 80 and overAgingAortic Valve StenosisCalcinosisCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell DifferentiationCell MovementClone CellsGenes, T-Cell Receptor betaHumansImmunophenotypingLymphocyte Activation

Identifiers

PMID21677140
PMCPMC3131440
OpenAlexW2170416037

What OpenQuestion holds

Textmetadata
LicenceTDM
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.