Evidence map›Paper›PMID 25887583›Full record

ArticleJournal of hematology & oncology2015

Soluble NKG2D ligand promotes MDSC expansion and skews macrophage to the alternatively activated phenotype.

Gang Xiao, Xuanjun Wang, Jun Sheng, Shengjun Lu, Xuezhong Yu, Jennifer D Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 56 citations in OpenAlex.

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  10. Soluble NKG2D ligands impair CD8Oncology letters · 2023
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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

6 authors at 2 institutions in 2 countries.

Gang XiaoDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA. xiaog@musc.edu.
Xuanjun WangKey Lab for Puer Tea Science, Ministry of Education, Yunnan Agricultural University, Kunming, China. wangxuanjun@gmail.com.
Jun ShengKey Lab for Puer Tea Science, Ministry of Education, Yunnan Agricultural University, Kunming, China.
Shengjun LuDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA. lussh@musc.edu.
Xuezhong YuDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA. yux@musc.edu.
Jennifer D WuDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA. wujjd@musc.edu.
Medical University of South Carolina · USYunnan Agricultural University · CN

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
Targeting MIC shedding to revive host NKG2D-mediated immune response in prostateR01CA149405 · NCI · UNIVERSITY OF WASHINGTON · PI WU, JENNIFER D · 2010 to 2014
$1.5M
NCI NIH HHS 1R01CA149405NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA149405
6 · The paper itself

Abstract

Expression of surface NKG2D ligand MIC on tumor cells is deemed to stimulate NK and co-stimulate CD8 T cell anti-tumor immunity. Human cancer cells however frequently adopt a proteinase-mediated shedding strategy to generate soluble MIC (sMIC) to circumvent host immunity. High levels of sMIC have been shown to correlate with advanced disease stages in cancer patients. The underlying mechanism is currently understood as systemic downregulation of NKG2D expression on CD8 T and NK cells and perturbing NK cell periphery maintenance. Herein we report a novel mechanism by which sMIC poses immune suppressive effect on host immunity and tumor microenvironment. We demonstrate that sMIC facilitates expansion of myeloid-derived suppressor cells (MDSCs) and skews macrophages to the more immune suppressive alternative phenotype through activation of STAT3. These findings further endorse that sMIC is an important therapeutic target for cancer immunotherapy.

Indexed as

AnimalsCell DifferentiationFlow CytometryHistocompatibility Antigens Class IHumansMacrophagesMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicMyeloid CellsPhenotypeTumor EscapeTumor MicroenvironmentHistocompatibility Antigens Class IMICB antigen

Identifiers

PMID25887583
PMCPMC4342005
OpenAlexW2096625852

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.