Evidence map›Paper›PMID 28258697›Full record

ReviewImmunological reviews2017

Tim-3 and its role in regulating anti-tumor immunity.

Madhumita Das, Chen Zhu, Vijay K Kuchroo

Abstract readReview
In one paragraph

Review in Immunological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 534 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
534citing papers in PubMed, 1 pooled it
24.0field-weighted citation impact, top 1% 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

534 citing papers in PubMed, 1 synthesis or guideline pooled it, 824 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Combined Targeting of PD-1 and TIM-3 in Patients with Locally Advanced or Metastatic Non-Small Cell Lung Cancer: AMBER Part 2B.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Trial
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  17. Improved Systemic Immunochemotherapy Employing an Oxaliplatin-TLR7/8 Agonist Prodrug Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  19. Review
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474 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Madhumita DasEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA.
Chen ZhuDiscovery Biology, Research and Development, Sanofi US, Cambridge, MA, USA.
Vijay K KuchrooEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA.
Brigham and Women's Hospital · USBroad Institute · USSanofi (United States) · US

Funding

Transgenic / Knock-out mouse coreP01AI073748 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BEHAR, SAMUEL M · 2008 to 2019
$17.1M
Role of Th1 specific cell surface molecule Tim-3 in EAE.R01NS045937 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI KUCHROO, VIJAY K. · 2003 to 2016
$4.9M
NIAID NIH HHS P01 AI073748NINDS NIH HHS R01 NS045937
6 · The paper itself

Abstract

Immunotherapy is being increasingly recognized as a key therapeutic modality to treat cancer and represents one of the most exciting treatments for the disease. Fighting cancer with immunotherapy has revolutionized treatment for some patients and therapies targeting the immune checkpoint molecules such as CTLA-4 and PD-1 have achieved durable responses in melanoma, renal cancer, Hodgkin's diseases and lung cancer. However, the success rate of these treatments has been low and a large number of cancers, including colorectal cancer remain largely refractory to CTLA-4 and PD-1 blockade. This has provided impetus to identify other co-inhibitory receptors that could be exploited to enhance response rates of current immunotherapeutic agents and achieve responses to the cancers that are refectory to immunotherapy. Tim-3 is a co-inhibitory receptor that is expressed on IFN-g-producing T cells, FoxP3+ Treg cells and innate immune cells (macrophages and dendritic cells) where it has been shown to suppress their responses upon interaction with their ligand(s). Tim-3 has gained prominence as a potential candidate for cancer immunotherapy, where it has been shown that in vivo blockade of Tim-3 with other check-point inhibitors enhances anti-tumor immunity and suppresses tumor growth in several preclinical tumor models. This review discusses the recent findings on Tim-3, the role it plays in regulating immune responses in different cell types and the rationale for targeting Tim-3 for effective cancer immunotherapy.

Indexed as

AnimalsAntigens, NeoplasmForkhead Transcription FactorsHepatitis A Virus Cellular Receptor 2HumansImmunityImmunomodulationImmunotherapyInterferon-gammaNeoplasmsT-Lymphocytes, RegulatoryTumor EscapeAntigens, NeoplasmForkhead Transcription FactorsFOXP3 protein, humanHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2Interferon-gammacheckpoint blockadecheckpoint inhibitorsimmunotherapyT cell exhaustionTim-3tumor immunity

Identifiers

PMID28258697
PMCPMC5512889
OpenAlexW2593059553

What OpenQuestion holds

Textmetadata
LicenceTDM
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.