Evidence map›Paper›PMID 30068593›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2018

Glatiramer Acetate Enhances Myeloid-Derived Suppressor Cell Function via Recognition of Paired Ig-like Receptor B.

William van der Touw, Kyeongah Kang, Yi Luan, Ge Ma, Sunny Mai, Lihui Qin, Guanglin Bian, Ruihua Zhang, Sathish Kumar Mungamuri, Hong-Ming Hu and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 20 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

16 authors at 7 institutions in 3 countries.

William van der TouwDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Kyeongah KangDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.ORCID 0000-0002-4465-0617
Yi LuanDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Ge MaDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Sunny MaiDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Lihui QinDepartment of Pathology, Weill Cornell Medical College, New York, NY 10065.
Guanglin BianDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Ruihua ZhangDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Sathish Kumar MungamuriDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Hong-Ming HuLaboratory of Cancer Immunobiology, Earle A. Chiles Research Institute, Providence Portland Medical Center, Portland, OR 97213.ORCID 0000-0002-2206-3470
Cheng Cheng ZhangDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Stuart A AaronsonDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Marc FeldmannKennedy Institute of Rheumatology, Nuffield Department of Orthopedics, Rheumatology, and Musculoskeletal Science, University of Oxford, Oxford OX3 7FZ, United Kingdom.
Wen-Chin YangAgricultural Biotechnology Research Center, Academia Sinica, Taipei 115, Taiwan.
Shu-Hsia ChenDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029; shuhsia.chen@houstonmethodist.org ppan@houstonmethodist.org.
Ping-Ying PanDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029; shuhsia.chen@houstonmethodist.org ppan@houstonmethodist.org.
Icahn School of Medicine at Mount Sinai · USHouston Methodist · USAgricultural Biotechnology Research Center, Academia Sinica · TWCornell University · USNuffield Orthopaedic Centre · GBProvidence Portland Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

TRAINING PROGRAM IN CANCER THERAPYT32CA078207 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI James J Manfredi · 1999 to 2026
$11.6M
Teaching biomedical and pharmacological trainees to produce FAIR data for AI & ML applicationsT32GM062754 · NIGMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI SCHLESSINGER, AVNER · 2001 to 2023
$6.2M
Intervention of immune tolerance by small molecules to enhance immune therapyR01CA127483 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, SHU-HSIA · 2008 to 2018
$3.4M
Myeloid Suppressor Cell-Mediated Immune Suppression of Tumor Specific T CellsR01CA109322 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHEN, SHU-HSIA · 2006 to 2015
$3.2M
Combination gene therapy for metastatic colon cancerR01CA070337 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CHEN, SHU-HSIA · 2002 to 2010
$2.7M
Modulation of tumor inflammatory factor for immune therapyR01CA208703 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, SHU-HSIA · 2017 to 2021
$2.3M
LILRB modulates tumor microenvironment and promotes tumor progressionR01CA204191 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, SHU-HSIA · 2017 to 2022
$2.2M
Novel therapy targeting refractory colon cancerR01CA188610 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI PAN, PING-YING · 2015 to 2019
$1.8M
HSC Derived MDSC for the Prevention of GHVD Without Suppressing GvLR01CA140243 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI PAN, PING-YING · 2011 to 2015
$1.7M
Myeloid suppressor cell-mediated immune suppressionR21DK073603 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CHEN, SHU-HSIA · 2005 to 2006
$419k
LILRB as a homeostatic regulator of human macrophage classical activationF32AI122715 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI VAN DER TOUW, WILLIAM · 2016 to 2016
$18k
NCI NIH HHS R01 CA070337NCI NIH HHS R01 CA109322NCI NIH HHS R01 CA127483NCI NIH HHS R01 CA140243NCI NIH HHS R01 CA188610NCI NIH HHS R01 CA204191NCI NIH HHS R01 CA208703NCI NIH HHS T32 CA078207NIAID NIH HHS F32 AI122715NIDDK NIH HHS R21 DK073603NIGMS NIH HHS T32 GM062754
6 · The paper itself

Abstract

Glatiramer acetate (GA; Copaxone) is a copolymer therapeutic that is approved by the Food and Drug Administration for the relapsing-remitting form of multiple sclerosis. Despite an unclear mechanism of action, studies have shown that GA promotes protective Th2 immunity and stimulates release of cytokines that suppress autoimmunity. In this study, we demonstrate that GA interacts with murine paired Ig-like receptor B (PIR-B) on myeloid-derived suppressor cells and suppresses the STAT1/NF-κB pathways while promoting IL-10/TGF-β cytokine release. In inflammatory bowel disease models, GA enhanced myeloid-derived suppressor cell-dependent CD4

Indexed as

AnimalsAntigens, CDAutoimmune DiseasesCytokinesFemaleGlatiramer AcetateHumansMiceMice, Inbred BALB CMice, KnockoutMyeloid-Derived Suppressor CellsNF-kappa BReceptors, ImmunologicTh2 CellsT-Lymphocytes, RegulatoryAntigens, CDCytokinesGlatiramer AcetateLILRB3 protein, humanNF-kappa BPirb protein, mouseReceptors, Immunologic

Identifiers

PMID30068593
PMCPMC6379207
OpenAlexW2887340421

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.