Evidence map›Paper›PMID 31160756›Full record

ArticleCellular & molecular immunology2020

Spatial distribution of IL4 controls iNKT cell-DC crosstalk in tumors.

Lu Wang, Zhilan Liu, Lili Wang, Qielan Wu, Xiang Li, Di Xie, Huimin Zhang, Yongdeng Zhang, Lusheng Gu, Yanhong Xue and 6 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Methods for Controlling Small GTPase Activity.Chembiochem : a European journal of chemical biology · 2025
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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 4 institutions in 1 country.

Lu Wang *Division of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Zhilan Liu *Division of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Lili WangDivision of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Qielan WuDivision of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Xiang LiDivision of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Di XieDivision of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Huimin ZhangDivision of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Yongdeng ZhangNational Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Lusheng GuNational Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Yanhong XueNational Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Ting YueSchool of Life Sciences, University of Science and Technology of China, 230027, Hefei, China.
Gang LiuNational Synchrotron Radiation Laboratory, University of Science and Technology of China, 230027, Hefei, China.
Wei JiNational Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Haiming WeiDivision of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China.
Tao XuNational Key Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, 100101, Beijing, China.
Li BaiDivision of Life Sciences and Medicine, Department of Oncology of The First Affiliated Hospital, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, China. baili@ustc.edu.cn.
University of Science and Technology of China · CNChinese Academy of Sciences · CNInstitute of Biophysics · CNNational Synchrotron Radiation Laboratory · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The spatiotemporal distribution of cytokines orchestrates immune responses in vivo, yet the underlying mechanisms remain to be explored. We showed here that the spatial distribution of interleukin-4 (IL4) in invariant natural killer T (iNKT) cells regulated crosstalk between iNKT cells and dendritic cells (DCs) and controlled iNKT cell-mediated T-helper type 1 (Th1) responses. The persistent polarization of IL4 induced by strong lipid antigens, that is, α-galactosylceramide (αGC), caused IL4 accumulation at the immunological synapse (IS), which promoted the activation of the IL4R-STAT6 (signal transducer and activator of transcription 6) pathway and production of IL12 in DCs, which enhanced interferon-γ (IFNγ) production in iNKT cells. Conversely, the nonpolarized secretion of IL4 induced by Th2 lipid antigens with a short or unsaturated chain was incapable of enhancing this iNKT cell-DC crosstalk and thus shifted the immune response to a Th2-type response. The nonpolarized secretion of IL4 in response to Th2 lipid antigens was caused by the degradation of Cdc42 in iNKT cells. Moreover, reduced Cdc42 expression was observed in tumor-infiltrating iNKT cells, which impaired IL4 polarization and disturbed iNKT cell-DC crosstalk in tumors.

Indexed as

Animalscdc42 GTP-Binding ProteinDendritic CellsGalactosylceramidesHumansImmunological SynapsesInterleukin-4Mice, Inbred C57BLMicrotubule-Organizing CenterNatural Killer T-CellsNeoplasmsPaclitaxelReceptors, Interleukin-4Signal TransductionSTAT6 Transcription FactorTh1 Cellsalpha-galactosylceramidecdc42 GTP-Binding ProteinGalactosylceramidesInterleukin-4PaclitaxelReceptors, Interleukin-4STAT6 Transcription FactorCrosstalkDCIL4iNKTPolarizationSpatial distributionTumor

Identifiers

PMID31160756
PMCPMC7192838
OpenAlexW2948337876

What Socratic holds

Textmetadata
LicenceCC BY
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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.