ArticleCancer immunology, immunotherapy : CII2025
Pomalidomide enhances CAR-T cell therapeutic efficacy and remodels immune microenvironment in lymphoid malignancies.
Article in Cancer immunology, immunotherapy : CII, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Myeloid-derived suppressor cells in multiple myeloma: mechanistic insights and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundChimeric antigen receptor T cell (CAR-T) therapy achieves high remission rates in lymphoid malignancies, but its long-term efficacy is limited by poor persistence and T cell exhaustion. Pomalidomide, an immunomodulatory drug (IMiD), demonstrates clinical synergy with CAR-T therapy, yet the underlying mechanisms driving this potentiation remain poorly defined. This study aimed to elucidate how pomalidomide enhances CAR-T cell function and remodels the immune microenvironment to overcome therapeutic limitations.
methodsIn vitro assays (CCK-8, LDH, qPCR, ELISA, flow cytometry) and bulk RNA-seq assessed pomalidomide's effects on human CAR-T cells. In vivo efficacy was evaluated in myeloma xenograft models. Single-cell RNA sequencing (scRNA-seq) of PBMCs from a lymphoma patient post-CAR-T/pomalidomide assessed immune microenvironment remodeling.
resultsPomalidomide significantly enhanced CAR-T cell proliferation and cytotoxicity in an activation-dependent manner. It upregulated effector molecules (IL-2, IFN-γ) and chemokines (CXCL9-CXCL11), promoted central memory T cells (Tcm), and induced metabolic reprogramming while reducing exhaustion markers. In xenografts, combination therapy induced tumor regression and extended survival vs. CAR-T alone. scRNA-seq revealed pomalidomide-driven remodeling, characterized by increased T/NK cell proportions/activity and reduced myeloid-derived suppressor cell (MDSC) signatures.
conclusionsPomalidomide synergizes with CAR-T by directly enhancing CAR-T function (memory, cytokine/chemokine production, metabolic fitness, and reduced exhaustion) and remodeling the suppressive immune microenvironment (increased cytotoxic effectors, diminished MDSC activity). These findings provide a crucial mechanistic rationale for optimizing pomalidomide-CAR-T combinations in refractory lymphoid malignancies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.