Evidence map›Paper›PMID 42060360›Full record

ArticleJCI insight2026

PD-1-targeted IL-15 mutein activates CD8+ and CD4+ T cells in infection and cancer.

Isaraphorn Pratumchai, Marie Bernardo, Julien Tessier, Jaroslav Zak, Kristi L Marquardt, Joon Sang Lee, Maheeka Bimal, AHyun Choi, Anthony M Byers, Mikielia G Devonish and 13 more

Abstract read
In one paragraph

Article in JCI insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

23 authors.

Isaraphorn PratumchaiThe Scripps Research Institute, Department of Immunology and Microbiology, La Jolla, California, USA.
Marie BernardoSanofi, Cambridge, Massachusetts, USA.
Julien TessierSanofi, Cambridge, Massachusetts, USA.
Jaroslav ZakThe Scripps Research Institute, Department of Immunology and Microbiology, La Jolla, California, USA.
Kristi L MarquardtThe Scripps Research Institute, Department of Immunology and Microbiology, La Jolla, California, USA.
Joon Sang LeeSanofi, Cambridge, Massachusetts, USA.
Maheeka BimalThe Scripps Research Institute, Department of Immunology and Microbiology, La Jolla, California, USA.
AHyun ChoiSanofi, Cambridge, Massachusetts, USA.
Anthony M ByersSanofi Vaccines, Orlando, Florida, USA.
Mikielia G DevonishSanofi Vaccines, Orlando, Florida, USA.
Roberto CarrioSanofi Vaccines, Orlando, Florida, USA.
Dan LuKadmon Corporation, A Sanofi Company, New York, New York, USA.
Stella MartomoKadmon Corporation, A Sanofi Company, New York, New York, USA.
Jeegar PatelKadmon Corporation, A Sanofi Company, New York, New York, USA.
Yu-An ZhangSanofi, Cambridge, Massachusetts, USA.
Ingeborg M LangohrSanofi, Cambridge, Massachusetts, USA.
Virna Cortez-RetamozoSanofi, Cambridge, Massachusetts, USA.
Dinesh S BangariSanofi, Cambridge, Massachusetts, USA.
Angela HadjipanayisSanofi, Cambridge, Massachusetts, USA.
Xiangming LiSanofi, Cambridge, Massachusetts, USA.
Valeria R FantinSanofi, Cambridge, Massachusetts, USA.
Donald R ShafferSanofi, Cambridge, Massachusetts, USA.
John R TeijaroThe Scripps Research Institute, Department of Immunology and Microbiology, La Jolla, California, USA.

Funding

The role of IL-27 in sustaining the exhausted CD8 T cell response to persistent infection and cancer.R01AI164744 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI TEIJARO, JOHN ROSS · 2021 to 2025
$2.7M
Reprogramming myeloid cells by JAK inhibition to enhance checkpoint blockade therapyK22CA292568 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jaroslav Zak · 2025 to 2026
$367k
NCI NIH HHS K22 CA292568NIAID NIH HHS R01 AI164744
6 · The paper itself

Abstract

Immune checkpoint inhibitors have transformed cancer therapy, yet many patients fail to achieve durable responses due to insufficient T cell reinvigoration. Cytokines offer promise for enhancing immunotherapy, but their clinical use is limited by toxicity and a narrow therapeutic index. Immunocytokines, engineered fusion proteins combining antibody specificity with cytokine activity, aim to overcome these challenges by targeting cytokine delivery to immune cells or the tumor microenvironment. We describe SAR445877 (SAR'877), a potentially novel PD-1-targeted immunocytokine that fuses a high-affinity anti-PD-1 antibody with a detuned IL-15/IL-15Rα sushi domain complex. SAR'877 blocks PD-1/PD-L1 and PD-1/PD-L2 interactions while selectively delivering IL-15 signals to PD-1+ T cells, enhancing proliferation and activation of antigen-experienced CD8+ and CD4+ T cells and NK cells, while minimizing systemic inflammation. Mechanistically, SAR'877 activates STAT5 signaling in PD-1+ lymphocytes and restores effector function in exhausted T cells. In preclinical models, a murine surrogate of SAR'877 accelerated viral clearance and induced robust antitumor immunity by expanding cytotoxic CD8+ T cells and promoting Th1 polarization. Notably, SAR'877 outperformed anti-PD-1 plus untargeted IL-15, highlighting the therapeutic potential of targeted IL-15 delivery. These findings position SAR'877 as a promising next-generation immunotherapy with enhanced efficacy and reduced cytokine-associated toxicities.

Indexed as

CD4-Positive T-LymphocytesCD8-Positive T-LymphocytesInterleukin-15NeoplasmsProgrammed Cell Death 1 ReceptorAnimalsFemaleHumansImmunotherapyMiceMice, Inbred C57BLT-Cell ExhaustionTumor MicroenvironmentIL15 protein, humanInterleukin-15PDCD1 protein, humanProgrammed Cell Death 1 ReceptorCancer immunotherapyCytokinesImmunologyImmunotherapyOncology

Identifiers

PMID42060360
PMCPMC13313502

What OpenQuestion holds

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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 OpenQuestion graph.