Evidence map›Paper›PMID 32222966›Full record

ArticleEuropean journal of immunology2020

TIM-3 and CEACAM1 do not interact in cis and in trans.

Annika De Sousa Linhares, Florian Kellner, Sabrina Jutz, Gerhard J Zlabinger, Hans-Joachim Gabius, Johannes B Huppa, Judith Leitner, Peter Steinberger

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. TIM-3+ Macrophages: Insights into Their Role in Cancer and Inflammation.International journal of molecular sciences · 2026
    Review
  4. Evolution of CEACAM pathogen decoy receptors in primates.European journal of clinical investigation · 2024
    Article
  5. LAG-3-An incompletely understood target in cancer therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. BTLA inhibition has a dominant role in theFrontiers in immunology · 2022
    Article
  13. Review
  14. Article
  15. Article
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  17. 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

8 authors at 3 institutions in 3 countries.

Annika De Sousa LinharesDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Florian KellnerInstitute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-5931-3798
Sabrina JutzDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Gerhard J ZlabingerDivision of Clinical and Experimental Immunology, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-7478-4173
Hans-Joachim GabiusFaculty of Veterinary Medicine, Institute for Physiological Chemistry, Ludwig-Maximilians-University, Munich, Germany.
Johannes B HuppaInstitute for Hygiene and Applied Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-2634-8198
Judith LeitnerDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-7156-1759
Peter SteinbergerDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-6848-4097
Medical University of Vienna · ATZero to Three · USLudwig-Maximilians-Universität München · DE

Funding

Austrian Science Fund 1248-B30Austrian Science Fund P32411Austrian Science Fund FWF P 32411Vienna Science and Technology Fund LS14-030
6 · The paper itself

Abstract

TIM-3 has been considered as a target in cancer immunotherapy. In T cells, inhibitory as well as activating functions have been ascribed to this molecule. Its role may therefore depend on the state of T cells and on the presence of interaction partners capable to perform functional pairing. Carcinoembryonic antigen-related cell adhesion molecule (CEACAM1) has been proposed to bind TIM-3 and to regulate its function. Using a T cell reporter platform we confirmed CEACAM1-mediated inhibition, but CEACAM1 did not functionally engage TIM-3. TIM-3 and CEACAM1 coexpression was limited to a small subset of activated T cells. Moreover, results obtained in extensive binding studies were not in support of an interaction between TIM-3 and CEACAM1. Cytoplasmic sequences derived from TIM-3 induced inhibitory signaling in our human T cell reporter system. Our results indicate that TIM-3 functions are independent of CEACAM1 and that this receptor has the capability to promote inhibitory signaling pathways in human T cells.

Indexed as

Antigens, CDCell Adhesion MoleculesFluorescence Resonance Energy TransferHEK293 CellsHepatitis A Virus Cellular Receptor 2HumansJurkat CellsLymphocyte ActivationSignal TransductionT-LymphocytesAntigens, CDCD66 antigensCell Adhesion MoleculesHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2CEACAM1CoinhibitionCostimulationT-cell activationTIM-3

Identifiers

PMID32222966
PMCPMC7496933
OpenAlexW3014084978

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.