Evidence map›Paper›PMID 33299138›Full record

ReviewExperimental & molecular medicine2020

Interactions between tumor-derived proteins and Toll-like receptors.

Gun-Young Jang, Ji Won Lee, Young Seob Kim, Sung Eun Lee, Hee Dong Han, Kee-Jong Hong, Tae Heung Kang, Yeong-Min Park

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
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  14. EngineeredMaterials today. Bio · 2025
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9 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

8 authors at 1 institution in 1 country.

Gun-Young JangDepartment of Immunology, College of Medicine, Konkuk University, 268 Chungwon-daero Chungju-si Chungcheongbuk-do, 27478, Seoul, South Korea.
Ji Won LeeDepartment of Immunology, College of Medicine, Konkuk University, 268 Chungwon-daero Chungju-si Chungcheongbuk-do, 27478, Seoul, South Korea.
Young Seob KimDepartment of Immunology, College of Medicine, Konkuk University, 268 Chungwon-daero Chungju-si Chungcheongbuk-do, 27478, Seoul, South Korea.
Sung Eun LeeDepartment of Immunology, College of Medicine, Konkuk University, 268 Chungwon-daero Chungju-si Chungcheongbuk-do, 27478, Seoul, South Korea.
Hee Dong HanDepartment of Immunology, College of Medicine, Konkuk University, 268 Chungwon-daero Chungju-si Chungcheongbuk-do, 27478, Seoul, South Korea.
Kee-Jong HongR&DB Foundation, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, South Korea.
Tae Heung KangDepartment of Immunology, College of Medicine, Konkuk University, 268 Chungwon-daero Chungju-si Chungcheongbuk-do, 27478, Seoul, South Korea. kangiron@kku.ac.kr.
Yeong-Min ParkDepartment of Immunology, College of Medicine, Konkuk University, 268 Chungwon-daero Chungju-si Chungcheongbuk-do, 27478, Seoul, South Korea. immun3023@kku.ac.kr.
Konkuk University · KR

Funding

National Research Foundation of Korea (NRF) NRF-2016R1A5A2012284National Research Foundation of Korea (NRF) NRF-2018R1A2B6008455
6 · The paper itself

Abstract

Damage-associated molecular patterns (DAMPs) are danger signals (or alarmins) alerting immune cells through pattern recognition receptors (PRRs) to begin defense activity. Moreover, DAMPs are host biomolecules that can initiate a noninflammatory response to infection, and pathogen-associated molecular pattern (PAMPs) perpetuate the inflammatory response to infection. Many DAMPs are proteins that have defined intracellular functions and are released from dying cells after tissue injury or chemo-/radiotherapy. In the tumor microenvironment, DAMPs can be ligands for Toll-like receptors (TLRs) expressed on immune cells and induce cytokine production and T-cell activation. Moreover, DAMPs released from tumor cells can directly activate tumor-expressed TLRs that induce chemoresistance, migration, invasion, and metastasis. Furthermore, DAMP-induced chronic inflammation in the tumor microenvironment causes an increase in immunosuppressive populations, such as M2 macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). Therefore, regulation of DAMP proteins can reduce excessive inflammation to create an immunogenic tumor microenvironment. Here, we review tumor-derived DAMP proteins as ligands of TLRs and discuss their association with immune cells, tumors, and the composition of the tumor microenvironment.

Indexed as

Signal TransductionAlarminsAnimalsBiomarkers, TumorDisease SusceptibilityGene Expression Regulation, NeoplasticHumansImmunomodulationNeoplasm ProteinsNeoplasmsOrgan SpecificityProtein BindingToll-Like ReceptorsTumor MicroenvironmentAlarminsBiomarkers, TumorNeoplasm ProteinsToll-Like Receptors

Identifiers

PMID33299138
PMCPMC8080774
OpenAlexW3111133036

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.