Evidence map›Paper›PMID 33352461›Full record

ArticleBiochemical and biophysical research communications2021

CEACAM1 specifically suppresses B cell receptor signaling-mediated activation.

Naoya Tsugawa, Daiki Yamada, Taro Watabe, Michio Onizawa, Shuang Wang, Yasuhiro Nemoto, Shigeru Oshima, Takeshi Tsubata, Takahiro Adachi, Yohei Kawano and 4 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2021. 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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 3 countries.

Naoya TsugawaDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Daiki YamadaDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Taro WatabeDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Michio OnizawaDepartment of Advanced Therapeutics for GI Diseases, Graduate School of Medical Science, TMDU, Tokyo, Japan.
Shuang WangDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan; Faculty of Medicine, Imperial College London, London, UK.
Yasuhiro NemotoDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan; Department of Advanced Therapeutics for GI Diseases, Graduate School of Medical Science, TMDU, Tokyo, Japan.
Shigeru OshimaDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Takeshi TsubataDepartment of Immunology, Medical Research Institute (MRI), TMDU, Tokyo, Japan.
Takahiro AdachiDepartment of Immunology, Medical Research Institute (MRI), TMDU, Tokyo, Japan.
Yohei KawanoDepartment of Immune Regulation, Graduate School of Medical Science, TMDU, Tokyo, Japan.
Mamoru WatanabeDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan; Advanced Research Institute, TMDU, Tokyo, Japan.
Richard S BlumbergGastroenterology Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Ryuichi OkamotoDepartment of Gastroenterology, Graduate School of Medical Science, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Takashi NagaishiDepartment of Advanced Therapeutics for GI Diseases, Graduate School of Medical Science, TMDU, Tokyo, Japan. Electronic address: tnagaishi.gast@tmd.ac.jp.
Tokyo Medical and Dental University · JPThe University of Tokyo · JPBrigham and Women's Hospital · USInstitute for Advanced Medical Research · US

Funding

Regulation of Mucosal LymphocytesR01DK051362 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg, Yu-Hwa Huang Blumberg · 1997 to 2026
$13.5M
MOLECULAR CHARACTERIZATION OF MUCOSAL LYMPHOCYTESR01DK044319 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg · 1992 to 2026
$10.4M
NIDDK NIH HHS R01 DK044319NIDDK NIH HHS R01 DK051362
6 · The paper itself

Abstract

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) expressed in T cells may regulate immune responses in the gut. In addition to T cells, B cells are also an important population in the gut-associated lymphoid tissues that orchestrate mucosal homeostasis. However, the role of CEACAM1 in B cells has not been elucidated. We herein analyzed mature B cells to determine the functions of CEACAM1. Flow cytometry revealed high expression of CEACAM1 on B cells in secondary lymphoid tissues. Cytokine production induced by activation of B cell receptor (BCR) signaling was suppressed by CEACAM1 signaling in contrast to that associated with either Toll-like receptor 4 or CD40 signaling. Confocal microscopy revealed co-localization of CEACAM1 and BCR when activated with anti-Igμ F(ab')

Indexed as

Signal TransductionAnimalsAntigens, CDB-LymphocytesCell Adhesion MoleculesCell DifferentiationCell LineageCells, CulturedCytokinesFemaleMiceMice, Inbred C57BLReceptors, Antigen, B-CellAntigens, CDCD66 antigensCell Adhesion MoleculesCytokinesReceptors, Antigen, B-CellB cellsBCR signalingCEACAM1Lymphoid tissuesSpontaneous proliferation

Identifiers

PMID33352461
PMCPMC9635307
OpenAlexW3117325332

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.