Evidence map›Paper›PMID 37427589›Full record

ArticleJCI insight2023

Reprogramming of PD-1+ M2-like tumor-associated macrophages with anti-PD-L1 and lenalidomide in cutaneous T cell lymphoma.

Zhen Han, Xiwei Wu, Hanjun Qin, Yate-Ching Yuan, Daniel Schmolze, Chingyu Su, Jasmine Zain, Lilach Moyal, Emmilia Hodak, James F Sanchez and 4 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

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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

14 authors at 6 institutions in 4 countries.

Zhen HanDivision of Dermatology.
Xiwei WuDepartment of Computational and Quantitative Medicine.
Hanjun QinDepartment of Computational and Quantitative Medicine.
Yate-Ching YuanDepartment of Computational and Quantitative Medicine.
Daniel SchmolzeDepartment of Pathology, and.
Chingyu SuDivision of Dermatology.
Jasmine ZainDepartment of Hematology and Hematopoietic Cell Transplantation, City of Hope, Duarte, California, USA.
Lilach MoyalDepartment of Dermatology, Rabin Medical Center, Felsenstein Medical Research Center, Tel Aviv University, Tel Aviv, Israel.
Emmilia HodakDepartment of Dermatology, Rabin Medical Center, Felsenstein Medical Research Center, Tel Aviv University, Tel Aviv, Israel.
James F SanchezBeckman Research Institute.
Peter P LeeBeckman Research Institute.
Mingye FengBeckman Research Institute.
Steven T RosenBeckman Research Institute.
Christiane QuerfeldDivision of Dermatology.
City of Hope · USBeckman Research InstituteQuantitative BioSciences · USInstitute of Genomics and Integrative Biology · INRabin Medical Center · ILTel Aviv University · IL

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI XIWEI WU · 1985 to 2026
$86.3M
Cutaneous T cell lymphoma: a paradigm for dissecting susceptibility and resistance to checkpoint inhibition therapyR01CA229510 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI QUERFELD, CHRISTIANE · 2019 to 2023
$2.8M
NCI NIH HHS P30 CA033572NCI NIH HHS R01 CA229510
6 · The paper itself

Abstract

Cutaneous T cell lymphoma (CTCL) is a disfiguring and incurable disease characterized by skin-homing malignant T cells surrounded by immune cells that promote CTCL growth through an immunosuppressive tumor microenvironment (TME). Preliminary data from our phase I clinical trial of anti-programmed cell death ligand 1 (anti-PD-L1) combined with lenalidomide in patients with relapsed/refractory CTCL demonstrated promising clinical efficacy. In the current study, we analyzed the CTCL TME, which revealed a predominant PD-1+ M2-like tumor-associated macrophage (TAM) subtype with upregulated NF-κB and JAK/STAT signaling pathways and an aberrant cytokine and chemokine profile. Our in vitro studies investigated the effects of anti-PD-L1 and lenalidomide on PD-1+ M2-like TAMs. The combinatorial treatment synergistically induced functional transformation of PD-1+ M2-like TAMs toward a proinflammatory M1-like phenotype that gained phagocytic activity upon NF-κB and JAK/STAT inhibition, altered their migration through chemokine receptor alterations, and stimulated effector T cell proliferation. Lenalidomide was more effective than anti-PD-L1 in downregulation of the immunosuppressive IL-10, leading to decreased expression of both PD-1 and PD-L1. Overall, PD-1+ M2-like TAMs play an immunosuppressive role in CTCL. Anti-PD-L1 combined with lenalidomide provides a therapeutic strategy to enhance antitumor immunity by targeting PD-1+ M2-like TAMs in the CTCL TME.

Indexed as

LenalidomideLymphoma, T-Cell, CutaneousTumor-Associated MacrophagesHumansImmunosuppressive AgentsMacrophagesNF-kappa BProgrammed Cell Death 1 ReceptorTumor MicroenvironmentImmunosuppressive AgentsLenalidomideNF-kappa BProgrammed Cell Death 1 ReceptorCancer immunotherapyDermatologyLymphomasMacrophages

Identifiers

PMID37427589
PMCPMC10371344
OpenAlexW4383682118

What OpenQuestion holds

Textmetadata
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.