Evidence map›Paper›PMID 40751812›Full record

ArticleCellular and molecular life sciences : CMLS2025

Blocking NKG2A in Echinococcus multilocularis infection partially relieves impairment of NK cell function of the host.

Ayinuer Aierken, Aili Aierken, Kalibixiati Aimulajiang, Abuduaini Abulizi, Zhongdian Yuan, Chang Liu, Dalong Zhu, Hanyue Zhao, Tuerganaili Aji

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Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

9 authors.

Ayinuer AierkenHepatobiliary & Hydatid Disease Department, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, Xinjiang Uyghur Autonomous Region, China.
Aili AierkenState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, Xinjiang, China.
Kalibixiati AimulajiangState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, Xinjiang, China.
Abuduaini AbuliziDepartment of Hepatobiliary and Hydatid Disease, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Zhongdian YuanDepartment of Hepatobiliary and Hydatid Disease, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Chang LiuDepartment of Hepatobiliary and Hydatid Disease, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Dalong ZhuDepartment of Hepatobiliary and Hydatid Disease, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Hanyue ZhaoDepartment of Hepatobiliary and Hydatid Disease, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Tuerganaili AjiHepatobiliary & Hydatid Disease Department, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, Xinjiang Uyghur Autonomous Region, China. tuergan1@163.com.ORCID http://orcid.org/0009-0001-6790-1300

Funding

Natural Science Foundation of Xinjiang No.2022D01D17Science and Technology Department of Xinjiang Uygur Autonomous Region SKL-HIDCA-2021-4Xinjiang Uyghur Autonomous Region Key Laboratory Open Research Program SKL-HIDCA-2024-2
6 · The paper itself

Abstract

backgroundAlveolar echinococcosis (AE) is a fatal zoonotic parasitic disease with biological characteristics similar to cancer. Although previous studies have reported immune dysfunction of Natural Killer (NK) cells due to other inhibitory receptors in AE, limited research has been conducted on the role of Natural Killer cell protein Group 2-A (NKG2A) in human NK cells. METHODS AND

resultsOur study revealed upregulation of NKG2A expression in peripheral blood and liver tissue NK cells in patients with AE, which was accompanied by a decrease in the secretion of IFN-γ, TNF-α, and Granzyme B by these NK cells. When we blocked the NKG2A receptor during co-culture of NK cells with Echinococcus multilocularis (E. multilocularis) proteins in vitro, we observed increased secretion of IFN-γ, TNF-α, and Granzyme B by NK cells. This observation was further confirmed in an E. multilocularis-infected mice model, in which higher expression levels of NKG2A on NK cells were detected, accompanied by a reduction in IFN-γ, TNF-α and Granzyme B secretion from NK cells. Deletion of NK cells in an E. multilocularis-infected mice model clearly resulted in more aggressive disease progression. Conversely, blocking NKG2A on NK cells results in increased secretion of TNF-α, and Granzyme B by NK cells. Similar changes in NKG2A expression and NK cell quality were observed in a mice model of splenic NK cells, as well as the functional recovery of NK cells after blocking NKG2A.

conclusionOur results demonstrate the involvement of NKG2A in impaired NK cell function during E. multilocularis infection in both humans and mice, suggesting that targeting NKG2A through blockade has the potential to restore NK cell function against this infection.

Indexed as

EchinococcosisEchinococcus multilocularisKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily CAnimalsDisease Models, AnimalFemaleGranzymesHumansInterferon-gammaMaleMiceMice, Inbred C57BLTumor Necrosis Factor-alphaGranzymesInterferon-gammaKLRC1 protein, humanNK Cell Lectin-Like Receptor Subfamily CTumor Necrosis Factor-alphaAlveolar echinococcosisNK cellNKG2API3K-AKT

Identifiers

PMID40751812
PMCPMC12317963

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.