Evidence map›Paper›PMID 40042995›Full record

ArticleCancer research2025

Single-Cell Analyses Reveal a Functionally Heterogeneous Exhausted CD8+ T-cell Subpopulation That Is Correlated with Response to Checkpoint Therapy in Melanoma.

Kelly M Mahuron, Osmaan Shahid, Prachi Sao, Clinton Wu, Alexandra M Haugh, Laura A Huppert, Lauren S Levine, Margaret M Lowe, Michael Alvarado, Markee Micu and 8 more

Abstract read
In one paragraph

Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
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

18 authors.

Kelly M Mahuron *Department of Surgery, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-2544-5191
Osmaan Shahid *Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-3694-8480
Prachi Sao *Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0001-5346-6742
Clinton Wu *Department of Medicine, University of Arizona, Tucson, Arizona.ORCID 0009-0008-1223-2243
Alexandra M HaughDepartment of Medicine, University of California, San Francisco, San Francisco, California.ORCID 0009-0005-5796-5836
Laura A HuppertDepartment of Medicine, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-8512-5608
Lauren S LevineDepartment of Medicine, University of California, San Francisco, San Francisco, California.ORCID 0000-0001-5504-7736
Margaret M LoweDepartment of Dermatology, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-5623-7707
Michael AlvaradoDepartment of Surgery, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-6605-3725
Markee MicuDepartment of Medicine, University of California, San Francisco, San Francisco, California.ORCID 0009-0005-2907-688X
Katy K TsaiDepartment of Medicine, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-7705-1813
Melissa ChowHelen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-6501-3991
Meromit SingerDepartment of Immunology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-1755-3598
Jason M SchenkelDepartment of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0003-4641-6872
Arlene H SharpeDepartment of Immunology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-9736-2109
Michael D RosenblumDepartment of Dermatology, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-0462-5732
Kristen E PaukenDepartment of Immunology, The University of Texas MD Anderson Cancer Center, Houston, Texas.ORCID 0000-0002-4309-7880
Adil I DaudDepartment of Medicine, University of California, San Francisco, San Francisco, California.ORCID 0000-0002-6617-8421

Funding

Role of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI VIJAY K. KUCHROO · 1996 to 2026
$51.7M
Transgenic/KnockoutP01AI056299 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BLAZAR, BRUCE R · 2003 to 2023
$42.5M
Synergies among inhibitory receptors in tolerance, cancer & antiviral immunityP01AI108545 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Dario AA Vignali · 2015 to 2026
$30.8M
Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 2003 to 2019
$21.8M
Understanding and Overcoming T cell Immunosuppression in GlioblastomaP01CA236749 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI E. Antonio Chiocca · 2020 to 2026
$19.5M
The University of Texas MD Anderson Cancer Center SPORE in MelanomaP50CA221703 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WARGO, JENNIFER A. · 2019 to 2023
$10.3M
Elucidating the Role of Regulatory T cells in Establishing and Maintaining a Th2 Niche in SkinR01AR077553 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSENBLUM, MICHAEL DAVID · 2020 to 2024
$3.5M
RESEARCH TRAINING IN GASTROINTESTINAL SURGERYT32DK007573 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HARRIS, HOBART WHITAKER · 1988 to 2019
$3.0M
UCSF Paul Calabresi K12 Career Development Program in Clinical OncologyK12CA260225 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BERGSLAND, EMILY K, BIVONA, TREVER G · 2021 to 2025
$2.6M
Elucidating the Cellular and Molecular Mechanisms of How Regulatory T cells in Skin Regulate Fibroblast Activation and Tissue FibrosisR01AR071944 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSENBLUM, MICHAEL DAVID · 2018 to 2022
$1.7M
The ontogeny and function of CD8 T cells in lung cancerK08CA256044 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SCHENKEL, JASON M. · 2021 to 2025
$1.1M
BD FACSAria Fusion Cell SorterS10OD021822 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEE, MICHAEL R. · 2016 to 2016
$573k
National Cancer Institute (NCI) P50CA221703National Institutes of Health (NIH) 5T32DK007573National Institutes of Health (NIH) 7K08CA256044-3National Institutes of Health (NIH) P01AI039671NCI NIH HHS K08 CA256044NCI NIH HHS K12 CA260225NCI NIH HHS P01 CA236749NCI NIH HHS P50 CA221703NIAID NIH HHS P01 AI039671NIAID NIH HHS P01 AI056299NIAID NIH HHS P01 AI108545NIAMS NIH HHS R01 AR071944NIAMS NIH HHS R01 AR077553NIDDK NIH HHS P30 DK063720NIDDK NIH HHS T32 DK007573NIH HHS S10 OD021822
6 · The paper itself

Abstract

PD-1 pathway inhibitors have revolutionized cancer therapy. However, most patients do not durably benefit, highlighting the need for biomarkers to stratify patients as responders or nonresponders. Although CD8+ tumor-infiltrating lymphocytes (TIL) have been associated with immune checkpoint therapy response, there is no consensus on which CD8+ TIL subpopulations have the most prognostic value. Preclinical studies have focused on progenitor-like exhausted CD8+ T cells (TPEX) because TPEX proliferate more in response to PD-1 inhibitors than other exhausted T-cell (TEX) subpopulations. However, immune checkpoint inhibitor treatment drives TPEX differentiation into other TEX populations that can mediate antitumor immunity. These data complicate the ability to identify prognostically important T-cell populations in patients that predict immune checkpoint inhibitor treatment response. In this study, we found that patients with advanced melanoma with ≥20% of CD8+ TILs coexpressing PD-1 and CTLA4 (termed CPHi TIL) had better objective response rates and survival following PD-1 monotherapy than those below this threshold. Characterization of the CPHi TIL subset using bulk and single-cell RNA sequencing showed that although TPEX-like cells were present within the CPHi subset, they were in the minority of these cells. Rather, the CPHi population was numerically dominated by other subsets, including cycling, terminally exhausted-like, cytotoxic-like, and/or resident memory-like TEX populations, and a subset enriched for glycolytic genes. Collectively, these data show that CPHi TILs correlate with response in melanoma, but this TIL subset is a heterogeneous mix of different subpopulations that may differentially contribute to antitumor immunity following checkpoint blockade. Significance: The PD-1+ CTLA4+ CD8+ tumor-infiltrating lymphocyte population correlating with immunotherapy response is a heterogeneous mix of subpopulations, which has important implications for optimizing checkpoint-based immunotherapy.

Indexed as

CD8-Positive T-LymphocytesImmune Checkpoint InhibitorsLymphocytes, Tumor-InfiltratingMelanomaSingle-Cell AnalysisSkin NeoplasmsCTLA-4 AntigenFemaleHumansMaleMiddle AgedPrognosisProgrammed Cell Death 1 ReceptorCTLA-4 AntigenCTLA4 protein, humanImmune Checkpoint InhibitorsPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID40042995
PMCPMC12356630

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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.