Evidence map›Paper›PMID 39068159›Full record

ArticleNature communications2024

Targeting myeloid-derived suppressor cells promotes antiparasitic T-cell immunity and enhances the efficacy of PD-1 blockade (15 words).

Chuanshan Zhang, Hui Wang, Tuerganaili Aji, Zhide Li, Yinshi Li, Abidan Ainiwaer, Zibigu Rousu, Jing Li, Maolin Wang, Bingqing Deng and 10 more

Erratum issuedAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

  1. Review
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  6. Th17-driven CD8Cell death & disease · 2026
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  9. Editorial: Parasite-induced liver diseases, volume II.Frontiers in cellular and infection microbiology · 2026
    Article
  10. PD-L1Frontiers in immunology · 2026
    Article
  11. Article
  12. Article
  13. Imaging mass cytometry of the immune microenvironment in alveolar echinococcosis.Frontiers in cellular and infection microbiology · 2026
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Upregulation of CD244 promotes CD8Parasites & vectors · 2024
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Chuanshan Zhang *State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China. dashan0518@126.com.ORCID 0000-0002-3241-2224
Hui Wang *State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.ORCID 0000-0002-9308-6186
Tuerganaili Aji *Key Laboratory of High Incidence Disease Research in Xingjiang, Ministry of Education, Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Zhide Li *State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Yinshi LiState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Abidan AiniwaerState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Zibigu RousuState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Jing LiBasic Medical College, Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Maolin WangState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Bingqing DengState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Adilai DuolikunState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Xuejiao KangState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Xuran ZhengState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Qian YuState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Yingmei ShaoDepartment of Hepatic Hydatid and Hepatobiliary Surgery, Digestive and Vascular Surgery Centre, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Wenbao ZhangState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China.
Dominique A VuittonWHO-Collaborating Centre for the Prevention and Treatment of Human Echinococcosis, Department of Parasitology, University Bourgogne Franche-Comté (EA 3181) and University Hospital, Besançon, France.
Zhigang TianHefei National Research Center for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, P. R. China.ORCID 0000-0002-5512-6378
Haoyu SunHefei National Research Center for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, P. R. China. haoyusun@ustc.edu.cn.ORCID 0000-0002-7506-8806
Hao WenState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University; Clinical Medicine Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, P. R. China. Dr.wenhao@163.com.ORCID 0000-0001-7144-220X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82160396
6 · The paper itself

Abstract

Immune exhaustion corresponds to a loss of effector function of T cells that associates with cancer or chronic infection. Here, our objective was to decipher the mechanisms involved in the immune suppression of myeloid-derived suppressor cells (MDSCs) and to explore the potential to target these cells for immunotherapy to enhance checkpoint blockade efficacy in a chronic parasite infection. We demonstrated that programmed cell-death-1 (PD-1) expression was significantly upregulated and associated with T-cell dysfunction in advanced alveolar echinococcosis (AE) patients and in Echinococcus multilocularis-infected mice. PD-1 blockade ex vivo failed to reverse AE patients' peripheral blood T-cell dysfunction. PD-1/PD-L1 blockade or PD-1 deficiency had no significant effects on metacestode in mouse model. This was due to the inhibitory capacities of immunosuppressive granulocytic MDSCs (G-MDSCs), especially in the liver surrounding the parasite pseudotumor. MDSCs suppressed T-cell function in vitro in an indoleamine 2, 3 dioxygenase 1 (IDO1)-dependent manner. Although depleting MDSCs alone restored T-cell effector functions and led to some limitation of disease progression in E. multilocularis-infected mice, combination with PD-1 blockade was better to induce antiparasitic efficacy. Our findings provide preclinical evidence in support of targeting MDSC or combining such an approach with checkpoint blockade in patients with advanced AE. (200 words).

Indexed as

EchinococcosisEchinococcus multilocularisImmune Checkpoint InhibitorsMyeloid-Derived Suppressor CellsProgrammed Cell Death 1 ReceptorT-LymphocytesAdultAnimalsB7-H1 AntigenDisease Models, AnimalFemaleHumansImmunotherapyMaleMiceMice, Inbred C57BLB7-H1 AntigenImmune Checkpoint InhibitorsPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID39068159
PMCPMC11283557

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Registered trials

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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.