Evidence map›Paper›PMID 22821642›Full record

ArticleHepatology (Baltimore, Md.)2013

Scavenger receptor A restrains T-cell activation and protects against concanavalin A-induced hepatic injury.

Daming Zuo, Xiaofei Yu, Chunqing Guo, Hongxia Wang, Jie Qian, Huanfa Yi, Xiao Lu, Zhi-Ping Lv, John R Subjeck, Huiping Zhou and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2013. 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
1.9field-weighted citation impact, top 15% 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, 40 citations in OpenAlex.

  1. Article
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  5. Gr-1American journal of translational research · 2020
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  20. High molecular weight stress proteins: Identification, cloning and utilisation in cancer immunotherapy.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2013
    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

13 authors at 3 institutions in 2 countries.

Daming ZuoDepartment of Human and Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.
Xiaofei Yu
Chunqing Guo
Hongxia Wang
Jie Qian
Huanfa Yi
Xiao Lu
Zhi-Ping Lv
John R Subjeck
Huiping Zhou
Arun J Sanyal
Zhengliang Chen
Xiang-Yang Wang
Virginia Commonwealth University · USSouthern Medical University · CNRoswell Park Comprehensive Cancer Center · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Paula Daniela Bos · 1985 to 2026
$51.0M
Large heat shock proteins and their role in cancer therapyR01CA099326 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI REPASKY, ELIZABETH A, WANG, XIANG-YANG SHAWN · 2003 to 2020
$5.7M
Large Stress Proteins in Biology and MedicineR01CA154708 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI WANG, XIANG-YANG SHAWN · 2011 to 2015
$1.5M
Scavenger Receptor-A and Immune RegulationR01CA129111 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI WANG, XIANG-YANG SHAWN · 2007 to 2011
$1.2M
NCI NIH HHS CA129111NCI NIH HHS CA154708NCI NIH HHS P30 CA016059NCI NIH HHS P30 CA16059NCI NIH HHS R01 CA099326NCI NIH HHS R01 CA129111NCI NIH HHS R01 CA154708
6 · The paper itself

Abstract

unlabelledNegative feedback immune mechanisms are essential for maintenance of hepatic homeostasis and prevention of immune-mediated liver injury. We show here that scavenger receptor A (SRA/CD204), a pattern recognition molecule, is highly up-regulated in the livers of patients with autoimmune or viral hepatitis, and of mice during concanavalin A (Con A)-induced hepatitis (CIH). Strikingly, genetic SRA ablation strongly sensitizes mice to Con A-induced liver injury. SRA loss, increased mortality and liver pathology correlate with excessive production of IFN-γ and heightened activation of T cells. Increased liver expression of SRA primarily occurs in mobilized hepatic myeloid cells during CIH, including CD11b(+) Gr-1(+) cells. Mechanistic studies establish that SRA on these cells functions as a negative regulator limiting T-cell activity and cytokine production. SRA-mediated protection from CIH is further validated by adoptive transfer of SRA(+) hepatic mononuclear cells or administration of a lentivirus-expressing SRA, which effectively ameliorates Con A-induced hepatic injury. Also, CIH and clinical hepatitis are associated with increased levels of soluble SRA. This soluble SRA displays a direct T-cell inhibitory effect and is capable of mitigating Con A-induced liver pathology.

conclusionOur findings demonstrate an unexpected role of SRA in attenuation of Con A-induced, T-cell-mediated hepatic injury. We propose that SRA serves as an important negative feedback mechanism in liver immune homeostasis, and may be exploited for therapeutic treatment of inflammatory liver diseases.

Indexed as

AnimalsCells, CulturedChemical and Drug Induced Liver InjuryConcanavalin AHepatitis, AnimalInterferon-gammaLiverLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutScavenger Receptors, Class AT-LymphocytesConcanavalin AInterferon-gammaScavenger Receptors, Class A

Identifiers

PMID22821642
PMCPMC3491179
OpenAlexW2087971743

What OpenQuestion holds

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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.