Evidence map›Paper›PMID 32948597›Full record

ReviewScience advances2020

Revisiting the PD-1 pathway.

Nikolaos Patsoukis, Qi Wang, Laura Strauss, Vassiliki A Boussiotis

Open access · goldAbstract readReview
In one paragraph

Review in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 333 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
333citing papers in PubMed, 1 pooled it
23.2field-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

333 citing papers in PubMed, 1 synthesis or guideline pooled it, 507 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Biochemistry and biophysics reports · 2026
    Review
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  17. Programmed death-ligand 1 on ex vivo-expanded toll-like-receptor-Bregs prevents allograft rejection by Breg viability promotion, CD4American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
    Article
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273 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

4 authors at 1 institution in 1 country.

Nikolaos PatsoukisDivision of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.ORCID 0000-0001-8746-5692
Qi WangDivision of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.ORCID 0000-0001-8898-8508
Laura StraussDivision of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Vassiliki A BoussiotisDivision of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. vboussio@bidmc.harvard.edu.ORCID 0000-0002-3963-1518
Beth Israel Deaconess Medical Center · US

Funding

Advancing Treatment Outcomes in Malignant Glioma by Integrating Immunotherapy and Standard of Care using Genetically Engineered Mice that Recapitulate Molecular Feature of Human GliomaR01CA229784 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BOUSSIOTIS, VASSILIKI A, CHAREST, ALAIN · 2018 to 2022
$3.3M
The effects of PD-1 on tumor-mediated “emergency” myelopoiesis and fate commitment of myeloid cells: Implications for anti-tumor immunityR01CA238263 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BOUSSIOTIS, VASSILIKI A · 2020 to 2024
$3.1M
Improving anti-tumor T cell immunity by targeting LDH-A functions beyond the Warburg effectR01CA212605 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BOUSSIOTIS, VASSILIKI A · 2017 to 2021
$2.8M
Exploitation of PD1-mediated tolerogenic signals for the treatment of SLER21AR073494 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PATSOUKIS, NIKOLAOS · 2019 to 2020
$424k
NCI NIH HHS R01 CA212605NCI NIH HHS R01 CA229784NCI NIH HHS R01 CA238263NIAMS NIH HHS R21 AR073494
6 · The paper itself

Abstract

Programmed Death-1 (PD-1; CD279) is an inhibitory receptor induced in activated T cells. PD-1 engagement by its ligands, PD-L1 and PD-L2, maintains peripheral tolerance but also compromises anti-tumor immunity. Blocking antibodies against PD-1 or its ligands have revolutionized cancer immunotherapy. However, only a fraction of patients develop durable antitumor responses. Clinical outcomes have reached a plateau without substantial advances by combinatorial approaches. Thus, great interest has recently emerged to investigate, in depth, the mechanisms by which the PD-1 pathway transmits inhibitory signals with the goal to identify molecular targets for improvement of the therapeutic success. These efforts have revealed unpredictable dimensions of the pathway and uncovered novel mechanisms involved in PD-1 and PD-L1 regulation and function. Here, we provide an overview of the recent advances on the mechanistic aspects of the PD-1 pathway and discuss the implications of these new discoveries and the gaps that remain to be filled.

Identifiers

PMID32948597
PMCPMC7500922
OpenAlexW3087169700

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.