Evidence map›Paper›PMID 34373574›Full record

ArticleScientific reports2021

Tunable heat shock protein-mediated NK cell responses are orchestrated by STAT1 in Antigen Presenting Cells.

Abigail L Sedlacek, Lauren B Kinner-Bibeau, Yifei Wang, Alicia P Mizes, Robert J Binder

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

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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 2 countries.

Abigail L SedlacekDepartment of Immunology, University of Pittsburgh School of Medicine, University of Pittsburgh, E1058 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA, 15261, USA.
Lauren B Kinner-BibeauKromatiD Inc, Longmont, CO, 80501, USA.
Yifei WangTsinghua University, Medical School,, Beijing, 100084, China.
Alicia P MizesDepartment of Medicine, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Robert J BinderDepartment of Immunology, University of Pittsburgh School of Medicine, University of Pittsburgh, E1058 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA, 15261, USA. rjb42@pitt.edu.
University of Pittsburgh · USTsinghua University · CN

Funding

CD91 and cancer immunosurveillanceR01CA233803 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BINDER, ROBERT J · 2020 to 2024
$1.7M
Heat shock protein gp96 and Treg responsesR21AI132875 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BINDER, ROBERT J · 2018 to 2019
$392k
Heat shock proteins and modulation of immune responsesR21CA208833 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BINDER, ROBERT J · 2016 to 2017
$368k
NCI NIH HHS R01 CA233803NCI NIH HHS R21 CA208833NIAID NIH HHS R21 AI132875
6 · The paper itself

Abstract

The release of Heat Shock Proteins (HSPs) from aberrant cells can initiate immune responses following engagement of the HSPs with antigen presenting cells (APCs). This is an important mechanism for cancer immunosurveillance and can also be modeled by vaccination with HSPs through various routes, targeting specific APCs expressing the HSP receptor CD91. Immunological outcomes can be varied as a result of the broad expression of CD91 in different dendritic cell and macrophage populations. We investigated the cellular response of different APCs to the prototypical immunogenic HSP, gp96, in the context of Th1 immunity. Although APCs generally express similar levels of the HSP receptor CD91, we uncovered APC-distinct, downstream signaling pathways activating STAT1, and differential STAT1 induced genes. As a result of this differential and unique signaling we determined that gp96-activated macrophages, but not DCs are capable of activating NK cells to produce IFN-[Formula: see text]. These data demonstrate that different APC subsets elicit unique intracellular signaling responses to HSPs which result in different patterns of downstream cellular activation and immune responses. Collectively this provides a novel tunable and autochthonous immune response to extracellular HSPs which has important implications on the development of immunity to cancer and infectious disease, as well as homeostasis.

Indexed as

AnimalsAntigen-Presenting CellsCells, CulturedFemaleHeat-Shock ProteinsImmunityKiller Cells, NaturalLymphocyte ActivationMiceMice, Inbred C57BLNeoplasmsSignal TransductionSTAT1 Transcription FactorHeat-Shock ProteinsStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID34373574
PMCPMC8352880
OpenAlexW3190010125

What OpenQuestion holds

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LicenceCC BY
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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.