GITR is a costimulatory receptor belonging to the tumor necrosis factor receptor superfamily, expressed at high levels on activated T cells and, to a lesser degree, on regulatory T cells and certain innate immune populations. Engagement of GITR by its ligand, GITRL, delivers costimulatory signals that promote T cell proliferation, survival, and effector function while simultaneously undermining the suppressive capacity of regulatory T cells. These properties made GITR an attractive target for cancer immunotherapy, and multiple agonistic antibodies entered clinical evaluation in combination with checkpoint inhibitors such as anti–PD-1. However, the clinical results were consistently disappointing: despite encouraging activity in mouse models, human trials of first-generation GITR agonists failed to demonstrate meaningful efficacy. The new study addresses this translational gap by dissecting, at the cellular and structural level, what an effective GITR agonist must actually do inside a living tumor.

The central insight of the work concerns the fragment crystallizable (Fc) region of the antibody. Agonistic antibodies against TNF receptor superfamily members can engage Fc gamma receptors (FcγRs) expressed on myeloid cells, and the nature of this engagement—activating versus inhibitory, high-affinity versus low-affinity—profoundly shapes the biological outcome. The team engineered an anti-GITR antibody with an Fc domain optimized for selective interaction with specific activating Fc gamma receptors while minimizing engagement of the inhibitory receptor FcγRIIB. This optimization was designed to exploit the biology of cross-linking: in vivo, GITR signaling is most efficiently triggered when the receptor is clustered on the cell surface, and FcγR-expressing antigen-presenting cells can serve as the scaffold that drives this clustering. Rather than treating the Fc region as an inert carrier, the researchers treated it as an active pharmacological component whose receptor selectivity determines where and how GITR agonism occurs.

The functional heart of the study is the identification of a CD4 T cell–dendritic cell crosstalk axis as the critical mechanism through which the optimized antibody promotes antitumor immunity. Dendritic cells are the professional antigen-presenting cells of the immune system, and their interaction with CD4 T cells in tumor-draining lymph nodes and within the tumor microenvironment determines the quality of the ensuing adaptive response. When the Fc-optimized anti-GITR antibody engages activating FcγRs on dendritic cells, it concentrates GITR cross-linking precisely at the immunological synapse between the dendritic cell and the CD4 T cell. The stimulated CD4 T cells, in turn, provide help to the dendritic cells—a bidirectional communication reminiscent of the classical CD40–CD40L licensing pathway—resulting in dendritic cell maturation, enhanced costimulatory molecule expression, and improved priming of cytotoxic CD8 T cells. The antibody thus does not merely activate T cells indiscriminately; it amplifies a defined cellular partnership that is essential for generating a durable, tumor-specific cytotoxic response.

The investigators used a combination of genetically engineered mouse models, adoptive transfer experiments, and depletion studies to establish this mechanism. Mice lacking specific Fc gamma receptors failed to respond to the optimized antibody, confirming that the therapeutic activity was Fc-dependent rather than a consequence of direct receptor agonism alone. Selective depletion and conditional knockout approaches demonstrated that both the CD4 T cell compartment and the dendritic cell compartment were indispensable: removal of either arm abolished the antitumor effect. Single-cell and flow cytometric analyses of treated tumors revealed expansion of interferon-gamma–producing CD4 helper cells, increased dendritic cell activation signatures, and a subsequent influx and activation of CD8 T cells capable of killing tumor cells. The effector phase of the response, although initiated by CD4 T cells, ultimately depended on CD8-mediated tumor cell lysis, positioning the antibody as an orchestrator of the full antitumor immune cascade rather than a single-cell-type stimulant.

An additional dimension of the study concerns regulatory T cells. Because GITR is abundantly expressed on the Treg population, agonistic antibodies have the theoretical potential to activate the very cells that suppress antitumor immunity. Earlier GITR agonists showed evidence of Treg destabilization in mice, but translating this effect to humans proved difficult. The new data suggest that the dominant effect of the Fc-optimized antibody under physiological conditions is the selective enhancement of conventional CD4 T cell help through dendritic cell engagement, rather than direct modulation of Tregs. By restricting productive GITR clustering to sites where activating FcγR-bearing antigen-presenting cells interact with conventional T cells, the antibody achieves a degree of spatial and cellular selectivity that systemically administered, unmodified agonists cannot. This selectivity likely explains the favorable balance of efficacy observed without the systemic inflammatory toxicity that has plagued other TNF receptor superfamily agonists in the clinic.

The engineering logic also carries broader implications for the immunotherapy pipeline. Antibodies targeting OX40, CD137 (4-1BB), CD27, and other costimulatory TNF receptors have followed a similar trajectory—striking preclinical activity followed by clinical underperformance—and several groups have independently converged on the conclusion that Fc receptor engagement and valency are decisive variables. The Nature Cancer study provides one of the most complete mechanistic accounts of how these variables operate in the specific context of CD4 T cell–dendritic cell biology. It suggests that the field’s earlier failures may not reflect intrinsic limitations of the GITR target but rather inadequate pharmacology: an antibody that binds GITR but lacks the correct Fc profile cannot create the cellular context in which GITR signaling benefits the antitumor response.

From a translational standpoint, the findings arrive at a moment when combination strategies are increasingly favored. The crosstalk amplified by the optimized antibody is mechanistically complementary to checkpoint blockade: anti–PD-1 reinvigorates exhausted cytotoxic T cells, whereas the Fc-optimized anti-GITR antibody expands and licenses the helper and antigen-presenting cell axis that supplies those cytotoxic cells. Preclinical combination data described in the study indicate additive or synergistic tumor control when the GITR agonist is paired with checkpoint inhibitors, supporting the design of clinical trials in which helper-axis stimulation precedes or accompanies T cell reinvigoration. The work also provides biomarkers for patient selection: tumors rich in dendritic cells and CD4 T cell infiltration—the so-called immune-inflamed phenotype—are the most likely to benefit, whereas “cold” tumors lacking this cellular infrastructure may require priming strategies such as radiation, oncolytic viruses, or chemotherapy before GITR agonism can be effective.

The study’s structural and pharmacological details will be of intense interest to antibody engineers. Selective Fc optimization—achieved through amino acid substitutions in the CH2 domain of the Fc region that modulate affinity for individual Fc gamma receptor subtypes—has emerged as a general strategy, sometimes termed FcγR tuning. The present work demonstrates that the optimal tuning profile is not universal but target-specific: it depends on which myeloid cell populations reside in the tumor microenvironment, which FcγRs they express, and where agonist-induced clustering must occur to produce the desired immune outcome. For GITR, the answer proved to be a profile favoring engagement of activating receptors on dendritic cells while avoiding inhibitory receptor engagement that would dampen clustering. This level of mechanistic resolution is rarely achieved in immunotherapy development and reflects the study’s systematic comparison of antibody variants differing only in their Fc sequences.

Safety considerations remain central to any costimulatory agonist program. Systemic GITR activation carries risks of autoimmune-like pathology and nonspecific T cell activation, and first-generation clinical candidates were dose-limited by cytokine-related toxicities. The Fc-optimized design mitigates these risks by requiring FcγR-mediated presentation for full activity, effectively gating receptor activation to professional antigen-presenting cell niches rather than permitting antibody-induced clustering in the circulation. The preclinical toxicity profile reported in the study was favorable, with therapeutic indices suggesting a therapeutic window wide enough for clinical exploration. Whether human FcγR biology—with its different receptor repertoire and expression patterns compared with mice—will reproduce this selectivity is the central question that clinical testing must answer, and the authors discuss species differences in FcγR distribution as a key consideration for trial design.

In the broader arc of cancer immunotherapy, the study exemplifies a maturing discipline: moving beyond target identification toward mechanism-first antibody design. Rather than asking whether a receptor can be stimulated, the field increasingly asks where, when, in which cells, and through which accessory receptors stimulation must occur to generate therapeutic benefit. By demonstrating that an Fc-optimized GITR antibody converts a CD4 T cell–dendritic cell dialogue into a potent, CD8-mediated antitumor attack, the research team has not only rehabilitated a once-discarded target but also supplied a template for engineering the next generation of immune agonists—molecules designed from the outset to act through, rather than around, the cellular architecture of the immune system.

STING, short for stimulator of interferon genes, is a central component of the innate immune system. It detects signals associated with abnormal or damaged cells and activates a molecular pathway that culminates in the production of type I interferons and other inflammatory mediators. These signals can help antigen-presenting cells mature and can improve the ability of the immune system to recognize and destroy tumor cells. The same pathway, however, is broadly expressed across tissues and can cause systemic inflammation when activated indiscriminately. This has made STING an attractive but difficult target for vaccine development, particularly when agonists are administered together with mRNA antigens.

A major problem is that STING activation can suppress the translation of messenger RNA. mRNA vaccines must be translated efficiently after entering cells so that the encoded antigen can be produced and displayed to the immune system. If a STING agonist is activated too early, the resulting antiviral and inflammatory response can shut down protein synthesis before sufficient antigen is made. In effect, the immune system’s alarm may interfere with the vaccine’s ability to deliver its message. The Syn-STING design addresses this timing conflict by separating the stages of antigen production and innate immune stimulation within the same delivery system.

The lipid nanoparticles used in the study carry an mRNA template for the selected antigen, an mRNA template for full-length STING and a delayed-release form of DMXAA, a small-molecule STING agonist. Full-length STING is an integral membrane protein that normally resides in the endoplasmic reticulum and moves through intracellular membranes after activation. By supplying STING mRNA, the researchers sought to increase STING availability specifically in cells that receive the nanoparticle rather than activating the pathway throughout the body. This is particularly important because the natural mouse and human versions of STING do not respond identically to every agonist.

DMXAA illustrates that species-specific problem. The compound can activate mouse STING but does not efficiently stimulate the common human form of the protein. To make the experimental system more relevant to human biology, the researchers used humanized STING mouse models and, in some experiments, a human STING mutant engineered to respond to DMXAA. The activator was attached to a biodegradable linker that controls when the active molecule becomes available. This bioorthogonal-like arrangement was intended to keep DMXAA inactive during the early phase of nanoparticle uptake and antigen production, then release it locally as the linker breaks down inside the target cells.

The study tested the platform with two model antigens: the E7 oncoprotein from human papillomavirus and ovalbumin, a widely used laboratory antigen. E7 is commonly used in experimental cancer vaccines because it can serve as a target in tumors driven by high-risk HPV infection. Ovalbumin provides a well-characterized system for measuring antigen-specific immune responses. In both settings, the researchers examined whether the synchronized formulation could preserve antigen expression while producing the inflammatory signals needed to activate dendritic cells and other antigen-presenting cells.

Following intratumoral or subcutaneous administration, the nanoparticles were preferentially taken up by myeloid cells, a broad immune-cell group that includes dendritic cells, macrophages and related populations. This distribution helped concentrate the vaccine’s activity in cells capable of processing antigen and presenting peptide fragments to T lymphocytes. The delayed activation strategy also preserved the fidelity of antigen mRNA translation, allowing cells to produce the encoded protein before strong STING-driven translational suppression occurred. The investigators observed localized activation of the pathway in antigen-presenting cells rather than widespread stimulation across the body.

That localization appeared to reduce several unwanted effects seen with more broadly active STING agonists. The researchers reported that Syn-STING did not promote systemic differentiation of regulatory B cells, which can dampen immune responses, and did not cause substantial apoptosis among immune cells. These findings are significant because an agonist that causes excessive or poorly targeted inflammation may paradoxically weaken vaccination by damaging responding lymphocytes or expanding immunosuppressive populations. By concentrating activity in the cells that receive the vaccine, the platform aims to create a stronger local immune environment without imposing the same degree of systemic stress.

The resulting immune response was characterized by robust adaptive immunity and a T helper 1-biased profile. Th1 responses are generally associated with interferon-gamma production and the activation of cytotoxic T cells, which can recognize and kill cells presenting tumor-associated antigens. In tumor-bearing mice, vaccination with Syn-STING suppressed tumor growth and prolonged survival compared with less coordinated approaches. The researchers also detected negligible immunity directed against the introduced STING protein, an important observation because repeated administration could otherwise be limited by anti-STING antibodies or T cell responses against the engineered component.

Although the findings establish a promising preclinical framework, several questions remain before the technology can be evaluated in human cancer trials. Human STING biology is genetically diverse, and engineered responsiveness to DMXAA in mice does not automatically reproduce the behavior of naturally occurring human STING variants. The safety of expressing full-length STING from mRNA, the pharmacology of the biodegradable linker and the performance of the nanoparticles in human tissues will require detailed study. It will also be necessary to determine how the platform behaves after repeat dosing and whether tumor type, injection route or prior immune status alters its effectiveness. Even so, the work demonstrates how precise control over the timing, location and molecular identity of innate immune activation could help overcome one of the central obstacles facing mRNA cancer vaccines.

Subject of Research: Syn-STING lipid nanoparticle mRNA vaccines for localized STING activation and antitumor immunity

Article Title: Enhanced antitumor immunity of mRNA vaccines by bioorthogonal-like delayed activation of exogeneous STING

Article References: Qin, P., Qin, Q., Hao, Y. et al. “Enhanced antitumor immunity of mRNA vaccines by bioorthogonal-like delayed activation of exogeneous STING.” Nature Biotechnology (2026). https://doi.org/10.1038/s41587-026-03224-y

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41587-026-03224-y

Keywords: mRNA vaccines, lipid nanoparticles, STING, DMXAA, cancer immunotherapy, antitumor immunity, HPV E7, ovalbumin, T cell immunity, delayed drug release, innate immunity, vaccine adjuvants

The study presents a compelling case for the triple remodeling of the tumor microenvironment, a strategy that focuses on enhancing drug delivery while simultaneously disrupting the protective barriers that tumors utilize to evade immune surveillance. By employing lipid nanoparticles that are specifically designed to target folate receptors—a hallmark of many cancer cells—the delivery system significantly increases the uptake of therapeutic agents within malignant tissues. This mechanism hinges upon the ability of these nanoparticles to navigate the complex cellular landscape of tumors, ensuring that they release their cargo where it is needed most.

Central to this research is the dual-targeting of both VEGF (vascular endothelial growth factor) and PD-L1 (programmed death-ligand 1). VEGF is known for its role in promoting angiogenesis, thereby supporting tumor growth and survival. By silencing VEGF via siRNA, the researchers can potentially debilitate the tumor’s blood supply, depriving it of necessary nutrients and oxygen. On the other hand, the targeted modulation of PD-L1 serves to enhance the efficacy of T-cell responses against cancer cells, thereby facilitating a more vigorous immune attack.

Hyaluronidase has been strategically incorporated into this experimental framework, serving as an enabler for enhanced drug penetration and distribution within dense tumor stroma. By breaking down hyaluronic acid—a major component of the extracellular matrix—hyaluronidase effectively reduces barriers to diffusion, allowing the therapeutic nanoparticles to infiltrate deeper into tumor tissues where conventional therapies struggle to reach. This enzymatic remodeling represents a significant shift in the approach to chemotherapeutic and immunotherapeutic delivery.

The implications of this study extend beyond the immediate effects on tumor behavior. By utilizing this targeted combination therapy, researchers envision an environment in which tumors are not only subject to direct cytotoxic effects but are also reconditioned to become more “immunogenic”. Through this process, cancer cells may be reprogrammed to express more immunogenic markers, thereby attracting immune responses that have previously been thwarted by tumor evasion tactics.

Moreover, the findings contribute to a growing body of literature emphasizing the importance of the tumor microenvironment in dictating therapeutic outcomes. The study positions the tumor microenvironment not merely as a passive background but as an active player in cancer biology—one that can be strategically manipulated to favor therapeutic efficacy. This perspective warrants a paradigm shift in the design of future cancer treatment protocols, accommodating the nuanced interactions between cancer cells and their surrounding environment.

The research methodology employed in this study is equally noteworthy. The authors utilized rigorous in vitro and in vivo models to validate their hypotheses, employing advanced imaging techniques to track nanoparticle distribution and silencing efficiency across different tumor types. These methodologies not only affirm the robustness of the results but also pave the way for future investigations into various theranostic applications—therapeutic regimens that also deliver diagnostic capabilities.

Furthermore, it’s essential to contextualize these findings within the broader landscape of cancer immunotherapy. Current immune checkpoint inhibitors, while promising, have shown varied responses among patients. The integration of a multi-faceted approach, as demonstrated in this study, could enhance the predictability of patient responses, leading to more personalized and effective treatment plans. This personalized medicine approach aligns closely with contemporary trends in oncology, catering to the unique biological dynamics exhibited by individual tumors.

As the research community continues to navigate the complexities of cancer treatment, the work by Li et al. stands out as a hallmark of innovative thinking. Their insights lay a compelling groundwork for future clinical trials aimed at translating these findings into standard medical practice. The potential to combine targeted therapy with immunology-enhancing strategies could revolutionize how patients respond to cancer treatment, making once-difficult-to-treat tumors more manageable.

In summary, the research highlights the significant promise of combining hyaluronidase-assisted strategies with advanced lipid nanoparticle technology to achieve a new standard in tumor immunotherapy. The intricate interplay between treatment modalities exemplified in this study represents a promising avenue for enhanced therapeutic efficacy in oncology. As researchers build upon this foundation, a future where cancer treatments are more effective and personalized is not just a possibility—it’s becoming a reality.

This pioneering study has set the stage for further exploration and validation within clinical settings, and with the potential to improve patient outcomes significantly, it underscores the importance of continued vigilance and innovation within the realm of cancer therapeutics. Exciting advancements and nuanced understandings of cancer biology are on the horizon, and the efforts put forth by Li et al. may very well lead the charge toward transformative solutions in the fight against cancer.

The global scientific community eagerly anticipates the developments that will arise from this foundational work, as the translational impact of their findings could very well reshape our understanding and approach to cancer treatment in years to come.

In conclusion, the integration of innovative methodologies and dual-targeting strategies not only enriches the current discourse on cancer immunotherapy but also positions the research efforts of Li et al. at the forefront of the ongoing battle against cancer, offering renewed hope and potential pathways for patients battling this pervasive disease.

Subject of Research: Triple remodeling of tumor microenvironment for cancer immunotherapy

Article Title: Triple-remodeling of tumor microenvironment through hyaluronidase-assisted folate-targeted lipid nanoparticle-mediated siVEGF/siPD-L1 for enhanced tumor immunotherapy

Article References:

Li, X., Xue, H., Liu, Q. et al. Triple-remodeling of tumor microenvironment through hyaluronidase-assisted folate-targeted lipid nanoparticle-mediated siVEGF/siPD-L1 for enhanced tumor immunotherapy.
J Transl Med (2026). https://doi.org/10.1186/s12967-026-07697-y

Image Credits: AI Generated

DOI: 10.1186/s12967-026-07697-y

Keywords: immunotherapy, lipid nanoparticles, tumor microenvironment, VEGF, PD-L1, hyaluronidase, siRNA, cancer treatment

At the heart of this research lies a deep dive into tumor metabolism—the complex web of biochemical reactions that sustain the malignant cells’ survival and proliferation. It is well known that cancer cells adopt unique metabolic strategies, often shifting their reliance away from oxygen-dependent respiration toward glycolysis, even in oxygen-rich environments (the Warburg effect). This metabolic reprogramming not only fuels tumor growth but also actively shapes the tumor microenvironment to suppress effective immune activity. The current investigation disrupts this paradigm by probing the impact of mitochondrial uncoupling, a process that decouples electron transport from ATP generation in mitochondria, thereby altering energy production and metabolite profiles.

The team employed a low dose mitochondrial uncoupler—a class of compounds traditionally considered for weight loss and metabolic disease treatments—to subtly modulate mitochondrial function within tumor cells. Unlike high doses that can induce cytotoxicity, the calibrated low dose serves to rewire metabolic fluxes without overwhelming cellular systems. This nuanced intervention was found to profoundly reconfigure the tumor metabolome, deviating energy pathways in a manner that appears to reverse the immunosuppressive characteristics of the tumor microenvironment. The metabolic remodeling creates conditions conducive to an invigorated cytotoxic T lymphocyte (CTL) attack, particularly by amplifying the activity and infiltration of CD8+ T cells.

A striking observation from the experiments was an increased infiltration and activation of CD8+ T cells within the tumor milieu following treatment with the mitochondrial uncoupler. Cytotoxic CD8+ T cells are pivotal players in anti-tumor immunity, capable of directly killing cancer cells. Tumors often evade these immune effectors by creating hostile metabolic environments or expressing inhibitory ligands. By reshaping tumor metabolism, the uncoupler disrupts these immunosuppressive signals, improving T cell function and persistence at the tumor site. This finding underscores the remarkable interplay between cellular metabolism and immune response, highlighting metabolic intervention as a potential immunotherapeutic strategy.

Importantly, the study demonstrates that the benefits of mitochondrial uncoupling extend beyond metabolic reprogramming alone. The authors observed alterations in key metabolites that serve as signaling molecules, potentially enhancing antigen presentation and the recruitment of immune effectors. Such changes may boost the visibility of cancer cells to the immune system, facilitating an effective immune-mediated tumor clearance. These insights open the door to combination therapies where metabolic modulators synergize with established immunotherapies such as checkpoint inhibitors, potentially overcoming resistance mechanisms.

The methodology encompassed a suite of state-of-the-art metabolomic profiling techniques, employing mass spectrometry and nuclear magnetic resonance spectroscopy to detail shifts in metabolite concentrations and fluxes. Complementary cellular analyses evaluated immune cell populations, activation markers, and cytokine secretion profiles. This multidisciplinary approach provided a comprehensive view of how subtle interference at the mitochondrial level cascades through tumor metabolism to ultimately heighten anti-tumor immune responses.

Beyond the molecular intricacies, the implications of these findings resonate deeply in clinical oncology. The ability to boost endogenous T cell responses without resorting to broad-spectrum cytotoxic drugs or intensive genetic engineering of immune cells presents a more accessible and potentially safer approach. The low dose mitochondrial uncoupler strategy, if validated in further preclinical models and human trials, could enhance the efficacy of existing immunotherapies and provide new hope for patients with resistant or intractable cancers.

Equally critical is the notion that targeting tumor metabolism may sensitize tumors to immune clearance by modulating the metabolic competition within the microenvironment. Tumor cells often outcompete T cells for key nutrients such as glucose and amino acids, starving the immune cells and impairing their function. By recalibrating mitochondrial activity, the uncoupler may rebalance this metabolic tug-of-war, ensuring that CD8+ T cells receive adequate substrates to sustain their cytotoxic activity and longevity.

While mitochondria have traditionally been viewed simply as cellular powerhouses, this research dramatically expands their perceived role to include pivotal regulators of immune interactions in cancer. The approach leverages the mitochondria’s central position within cellular metabolism to orchestrate systemic changes that potentiate immune surveillance and destruction of malignant cells. This challenges conventional therapeutic strategies and reinvigorates interest in metabolic interventions in oncology.

The robustness of the CD8+ T cell response elicited by mitochondrial uncoupling also raises intriguing possibilities regarding memory T cell formation and long-term tumor immunity. Effective cancer immunotherapy not only requires immediate tumor clearance but also durable protection against recurrence. The metabolic environment shaped by the uncoupler could favor the generation or maintenance of memory T cells, potentially inducing lasting immunological vigilance.

Remarkably, the treatment’s efficacy depended heavily on fine-tuning the uncoupler dose; excessive mitochondrial uncoupling proved detrimental, underscoring the delicate balance between perturbing tumor metabolism and preserving systemic health. This precision medicine aspect highlights the need for further pharmacokinetic and safety evaluations but also suggests that mitochondrial targeting could be personalized for maximal therapeutic gain.

The authors emphasize that this research sets the stage for a new class of metabolic immunomodulators that harness mitochondrial dynamics as a therapeutic fulcrum. Future investigations are expected to explore the mechanistic underpinnings of metabolite changes, expand testing to diverse tumor types, and assess combinatorial regimens with immunomodulatory agents or chemotherapy. Such integrated approaches may unlock synergistic anti-tumor effects and reduce the likelihood of therapeutic resistance.

From a broader perspective, the study reinforces the concept that tumor metabolism and immunity are deeply interwoven, and that interventions targeting one axis are likely to influence the other profoundly. This dual targeting could overcome the significant barrier that tumor immunosuppression has posed in cancer therapy, enabling immune cells to exert their natural tumor-clearing capabilities more effectively.

In conclusion, Jiang et al.’s work represents a paradigm shift, revealing that metabolic remodeling via a low dose mitochondrial uncoupler is not simply a biochemical curiosity but a potent immunological tool capable of orchestrating robust anti-tumor responses. This discovery invites a reevaluation of metabolic drugs in cancer therapy and opens exciting avenues for innovative treatments designed to empower the immune system by harnessing the cell’s fundamental energy machinery.

Subject of Research: Tumor metabolome remodeling via mitochondrial uncoupling to enhance CD8+ T cell anti-tumor immunity.

Article Title: Tumor metabolome remolded by low dose mitochondrial uncoupler elicits robust CD8+ T cell response.

Article References: Jiang, X., Fan, Z., Zhang, Z. et al. Tumor metabolome remolded by low dose mitochondrial uncoupler elicits robust CD8+ T cell response. Cell Death Discov. 11, 291 (2025). https://doi.org/10.1038/s41420-025-02584-9

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41420-025-02584-9