Evidence map›Paper›PMID 28314758›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2017

Immune checkpoint dysfunction in large and medium vessel vasculitis.

Ryu Watanabe, Hui Zhang, Gerald Berry, Jörg J Goronzy, Cornelia M Weyand

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Thromboembolic events in giant cell arteritis: a scoping review.Annals of medicine and surgery (2012) · 2026
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6 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

5 authors at 1 institution in 1 country.

Ryu WatanabeDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California; and.
Hui ZhangDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California; and.
Gerald BerryDepartment of Pathology, Stanford University School of Medicine, Stanford, California.
Jörg J GoronzyDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California; and.
Cornelia M WeyandDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California; and cweyand@stanford.edu.
Stanford University · US

Funding

The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2016 to 2020
$12.4M
The NOTCH Signaling Pathway in Large Vessel VasculitisR01HL117913 · NHLBI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2025
$5.0M
Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
Telomere Damage Responses and Immune AgingR01AI108906 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2024
$4.0M
T Cell Signaling in Rheumatoid ArthritisI01BX001669 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI GORONZY, JORG J · 2012 to 2021
–
BLRD VA I01 BX001669NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R01 HL117913NIAID NIH HHS R01 AI108906NIAMS NIH HHS R01 AR042527
6 · The paper itself

Abstract

Giant cell arteritis (GCA) is a granulomatous vasculitis of the aorta and its medium-sized branch vessels. CD4 T cells, macrophages, and dendritic cells (DCs) build granulomatous infiltrates that injure the vessel wall and elicit a maladaptive response to injury. Pathological consequences include fragmentation of elastic membranes, destruction of the medial layer, microvascular neoangiogenesis, massive outgrowth of myofibroblasts, and lumen-occlusive intimal hyperplasia. Antigens have been suspected to drive the local activation of vasculitogenic CD4 T cells, but recent data have suggested a more generalized defect in the threshold setting of such T cells, rendering them hyperreactive. Under physiological conditions, immune checkpoints provide negative signals to curb T cell activation and prevent inflammation-associated tissue destruction. This protective mechanism is disrupted in GCA. Vessel wall DCs fail to express the immunoinhibitory ligand programmed cell death ligand-1, leaving lesional T cells unchecked. Consequently, programmed cell death protein-1-positive CD4 T cells can enter the immunoprivileged vessel wall, where they produce a broad spectrum of inflammatory cytokines (interferon-γ, IL-17, and IL-21) and have a direct role in driving intimal hyperplasia and intramural neoangiogenesis. The deficiency of the programmed cell death protein-1 immune checkpoint in GCA, promoting unopposed T cell immunity, contrasts with checkpoint hyperactivity in cancer patients in whom excessive programmed cell death ligand-1 expression paralyzes the function of antitumor T cells. Excessive checkpoint activity is the principle underlying cancer-immune evasion and is therapeutically targeted by immunotherapy with checkpoint inhibitors. Such checkpoint inhibitors, which unleash anticancer T cells and induce immune-related toxicity, may lead to drug-induced vasculitis.

Indexed as

AnimalsArteriesCD4-Positive T-LymphocytesCytokinesGiant Cell ArteritisHumansImmunity, InnateImmunologic FactorsModels, ImmunologicalSignal TransductionCytokinesImmunologic Factorsdendritic cellgiant cell arteritisimmune checkpointprogrammed cell death ligand-1programmed cell death protein-1

Identifiers

PMID28314758
PMCPMC5451585
OpenAlexW2597105572

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.