Evidence map›Paper›PMID 26277892›Full record

ArticleCellular & molecular immunology2017

Ligation of CD180 inhibits IFN-α signaling in a Lyn-PI3K-BTK-dependent manner in B cells.

Ming You, Guanjun Dong, Fanlin Li, Feiya Ma, Jing Ren, Yujun Xu, Huimin Yue, Ruijing Tang, Deshan Ren, Yayi Hou

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. CD20Frontiers in immunology · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
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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

10 authors at 1 institution in 1 country.

Ming YouThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Guanjun DongThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Fanlin LiThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Feiya MaThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Jing RenThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Yujun XuThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Huimin YueThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Ruijing TangThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Deshan RenThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Yayi HouThe State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, People's Republic of China.
Nanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A hallmark of systemic lupus erythematosus (SLE) is the consistent production of various auto-antibodies by auto-reactive B cells. Interferon-α (IFN-α) signaling is highly activated in SLE B cells and plays a vital role in the antibody response by B cells. Previous studies have shown that CD180-negative B cells, which are dramatically increased in SLE patients, are responsible for the production of auto-antibodies. However, the association between CD180 and IFN-α signaling remains unknown. In the present study, we explored the effect of CD180 on regulating the activation of IFN-α signaling in B cells. We found that the number of CD180-negative B cells was increased in MRL/Mp-Fas(lpr/lpr) lupus-prone mice compared with wild-type mice. Phenotypic analysis showed that CD180-negative B cells comprised CD138

Indexed as

Signal TransductionAgammaglobulinaemia Tyrosine KinaseAnimalsAntigens, CDB-LymphocytesDown-RegulationFemaleGene Expression RegulationHumansInterferon-alphaLupus Erythematosus, SystemicMice, Inbred C57BLMice, Inbred MRL lprPhenotypePhosphatidylinositol 3-KinasesPhosphotyrosineAgammaglobulinaemia Tyrosine KinaseAntigens, CDBTK protein, humanCD180 protein, humanInterferon-alphaLy78 protein, mouselyn protein-tyrosine kinasePhosphatidylinositol 3-KinasesPhosphotyrosineProtein-Tyrosine Kinasessrc-Family KinasesSTAT2 Transcription FactorToll-Like Receptor 7Toll-Like Receptor 9

Identifiers

PMID26277892
PMCPMC5301152
OpenAlexW1707658851

What OpenQuestion holds

Textmetadata
Read underepoch 390

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 OpenQuestion graph.