Evidence map›Paper›PMID 39786926›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

Anti-CTLA-4 generates greater memory response than anti-PD-1 via TCF-1.

Stephen Mok, Huey Liu, Didem Ağaç Çobanoğlu, Nana-Ama A S Anang, James J Mancuso, E John Wherry, James P Allison

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Cell surface ADGRG1 and CD86 expression identifies antitumor CD4Proceedings of the National Academy of Sciences of the United States of America · 2026
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  15. Terminally exhausted CD8Frontiers in immunology · 2025
    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

7 authors.

Stephen MokDepartment of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Huey LiuDepartment of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Didem Ağaç ÇobanoğluDepartment of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.
Nana-Ama A S AnangDepartment of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.ORCID 0000-0002-8495-2978
James J MancusoJames P. Allison Institute, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.ORCID 0000-0001-5776-8617
E John WherryDepartment of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia, PA 19104.ORCID 0000-0003-0477-1956
James P AllisonDepartment of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030.

Funding

Virology CoreU19AI082630 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Michela Locci · 2009 to 2026
$48.1M
Synergies among inhibitory receptors in tolerance, cancer & antiviral immunityP01AI108545 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI E. John Wherry · 2015 to 2026
$30.8M
Sequencing and Viral Evolution CoreU19AI117950 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WHERRY, E. JOHN · 2015 to 2019
$12.0M
Testing the role of BATF as a pioneer transcription factor in effector T cellsR01AI115712 · NIAID · DANA-FARBER CANCER INST · PI KADOCH, CIGALL, WHERRY, E. JOHN · 2015 to 2019
$2.9M
Temporal control of differentiation and epigenetics of Exhausted CD8 T cells by ToxR01AI155577 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WHERRY, E. JOHN · 2020 to 2024
$2.7M
Cancer Prevention and Research Institute of Texas (CPRIT) R1203HHS | NIH (NIH) AI155577 AI115712 AI117950 AI108545 AI082630NIAID NIH HHS P01 AI108545NIAID NIH HHS R01 AI115712NIAID NIH HHS R01 AI155577NIAID NIH HHS U19 AI082630NIAID NIH HHS U19 AI117950
6 · The paper itself

Abstract

The effects of T cell differentiation arising from immune checkpoint inhibition targeting cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) and programmed cell death protein 1 (PD-1) on the immunological memory response remain unclear. Our investigation into the effects of anti-CTLA-4 and anti-PD-1 on memory T cell formation in mice reveals that memory T cells generated by anti-CTLA-4 exhibit greater expansion, cytokine production, and antitumor activity than those from anti-PD-1. Notably, anti-CTLA-4 preserves more T cell factor-1 (TCF-1)+ T cells during priming, while anti-PD-1 leads to more thymocyte selection-associated high mobility group box (TOX)+ T cells. Experiments using conditional

Indexed as

CTLA-4 AntigenImmunologic MemoryMice, KnockoutProgrammed Cell Death 1 ReceptorAnimalsHepatocyte Nuclear Factor 1-alphaImmune Checkpoint InhibitorsMemory T CellsMiceMice, Inbred C57BLCTLA-4 AntigenCtla4 protein, mouseHepatocyte Nuclear Factor 1-alphaHnf1a protein, mouseImmune Checkpoint InhibitorsPdcd1 protein, mouseProgrammed Cell Death 1 Receptoranti-CTLA-4anti-PD-1immune checkpoint therapiesmemory response

Identifiers

PMID39786926
PMCPMC11745370

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.