Evidence map›Paper›PMID 23936099›Full record

ArticlePloS one2013

C5a regulates IL-12+ DC migration to induce pathogenic Th1 and Th17 cells in sepsis.

Ning Ma, Chen Xing, He Xiao, Yi Wang, Ke Wang, Chunmei Hou, Gencheng Han, Guojiang Chen, Bernadette Marrero, Yujuan Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  6. Intestinal microbiota: a new force in cancer immunotherapy.Cell communication and signaling : CCS · 2020
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  12. Antiseptic effect of sea cucumber (Experimental and therapeutic medicine · 2016
    Article
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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

13 authors at 4 institutions in 2 countries.

Ning MaLaboratory of Immunology, Institute of Basic Medical Sciences, Beijing, China.
Chen Xing
He Xiao
Yi Wang
Ke Wang
Chunmei Hou
Gencheng Han
Guojiang Chen
Bernadette Marrero
Yujuan Wang
Beifen Shen
Yan Li
Renxi Wang
Institute of Basic Medical Sciences of the Chinese Academy of Medical SciencesNational Eye Institute · USJilin University · CNNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIt is well known that complement system C5a is excessively activated during the onset of sepsis. However, it is unclear whether C5a can regulate dentritic cells (DCs) to stimulate adaptive immune cells such as Th1 and Th17 in sepsis.

methodsSepsis was induced by cecal ligation and puncture (CLP). CLP-induced sepsis was treated with anti-C5a or IL-12. IL-12(+)DC, IFNγ(+)Th1, and IL-17(+)Th17 cells were analyzed by flow cytometry. IL-12 was measured by ELISA.

resultsOur studies here showed that C5a induced IL-12(+)DC cell migration from the peritoneal cavity to peripheral blood and lymph nodes. Furthermore, IL-12(+)DC cells induced the expansion of pathogenic IFNγ(+)Th1 and IL-17(+)Th17 cells in peripheral blood and lymph nodes. Moreover, IL-12, secreted by DC cells in the peritoneal cavity, is an important factor that prevents the development of sepsis.

conclusionOur data suggests that C5a regulates IL-12(+)DC cell migration to induce pathogenic Th1 and Th17 cells in sepsis.

Indexed as

Cell MovementAnimalsCD11c AntigenCecumCell CountComplement C5aDendritic CellsDisease ProgressionInterleukin-12LigationLymph NodesMaleMiceMice, Inbred C57BLPeritoneal CavityProtective AgentsCD11c AntigenComplement C5aInterleukin-12Protective Agents

Identifiers

PMID23936099
PMCPMC3720656
OpenAlexW2057024357

What OpenQuestion holds

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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.