Evidence map›Paper›PMID 31870332›Full record

ArticleBMC cancer2019

Microbial antigens-loaded myeloma cells enhance Th2 cell proliferation and myeloma clonogenicity via Th2-myeloma cell interaction.

Faqing Tian, Bo Lu, Ziren Chen, Junru Liu, Delan Ji, Juheng Li, Meiqin Tang, Wei Zhu, Juan Li

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. 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
0.5field-weighted citation impact, top 34% 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, 8 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Faqing TianDepartment of Hematology, Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, Guangdong, China. trumantfq@163.com.ORCID http://orcid.org/0000-0003-3527-467X
Bo LuDepartment of Hematology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Ziren ChenDepartment of Hematological Oncology, Shenzhen University General Hospital, Shenzhen, 518055, China.
Junru LiuDepartment of Hematology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong, China.
Delan JiDepartment of Hematology, Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, Guangdong, China.
Juheng LiDepartment of Hematology, Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, Guangdong, China.
Meiqin TangDepartment of Hematology, Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, Guangdong, China.
Wei ZhuDepartment of Pathology, School of Basic Medicine, Guangdong Medical University, Dongguan, 523808, Guangdong, China.
Juan LiDepartment of Hematology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong, China. lijuan__happy@163.com.
Sun Yat-sen University · CNLonggang Central Hospital · CNGuangdong Medical College · CNShenzhen University · CN

Funding

National Natural Science Foundation of China No.81472275the Medical Research Foundation of Guangdong Province No. B2018150the Natural Science Foundation of Guangdong Province, China No.2014A030313542the Science and Technology R & D Fund of Shenzhen No. JCYJ20170307104838077
6 · The paper itself

Abstract

backgroundMyeloma cells retain B cell functions, considered to be potential antigen presenting cells, yet there is little information regarding promoting Th2 cell proliferation or the direct effects to myeloma on the Th2 cells stimulated by microbial antigens-loaded myeloma cells.

methodsMixed lymphocyte reaction was used colorimetric assays via CCK8-kit. Surface molecular expression was performed by flow cytometry, cells sorting using microbeads. The concentrations of cytokines in serum were assessed using an ELISA kit. Clonogenic assay were performed in a methylcellulose culture system. Statistical analysis was assessed using the Student's t-test or one-way analysis of variance for multiple comparisons test.

resultsThe expression of HLA-DR, CD80 and CD40 on RPMI8266 cell membrane surface was upregulated by interaction with interferon-γ and/or Bacillus Calmette-Guerin Vaccine (BCGV). RPMI8266 cells were able to induce the mixed lymphocyte reaction in a dose-dependent fashion. The Th2 ratio induced by RPMI8266 treated by BCGV and interferon-γ (treated-RPMI8266) cells was only slightly greater than by untreated-tumor cells, but the serum IL-4 level secreted by Th2 cells was markedly higher in treated-RPMI8266 cells group. Th2 cells stimulated by treated-myeloma cells could directly promote treated-myeloma cell clonogenicity in a dose-dependent manner. Anti-HLADR IgG2b completely blocked increased of IL-4 secretion by Th2 cells stimulated by treated-myeloma cells, while also blocked enhancing the clonogenicity of treated tumor cells stimulated by MM-Th2 cells.

conclusionsThese results indicate that a novel mechanism of myeloma pathogenesis in myeloma cells could act as an APC to present microbial Ags to Th2 cells, promoting Th2 cell proliferation, consequently facilitating tumor development by close interaction between Th2 myeloma cells. Taken together, the microbial Ag presenting course of MM-Th2-MM interactions-restricted by MHC class-II-may result in tumor development such that all factors involved in the system could have a potential for myeloma therapeutic intervention.

Indexed as

Antigen-Presenting CellsAntigens, BacterialCell CommunicationCell Line, TumorCell ProliferationCells, CulturedCytokinesHumansLymphocyte ActivationLymphocyte Culture Test, MixedMultiple MyelomaTh2 CellsAntigens, BacterialCytokinesAntigen presenting cellsClonogenicityMHC- II restrictionMicrobial antigenMyelomaTh2 cell

Identifiers

PMID31870332
PMCPMC6929311
OpenAlexW2997632294

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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.