Cerebral malaria, one of the most severe manifestations of the disease caused by Plasmodium falciparum, is notorious for its high mortality rate and debilitating neurological sequelae in survivors. Despite intense research, the immune dysregulation contributing to cerebral malaria’s pathogenesis has proven difficult to control therapeutically, leading to an urgent need for novel interventions. The current study explores an uncharted avenue—leveraging the immunomodulatory capabilities of MSCs, which have garnered increasing attention for their anti-inflammatory and tissue repair properties in various autoimmune and inflammatory diseases.

The key insight emerging from this research is the critical role of the immune axis between T helper 17 (Th17) cells and regulatory T cells (Tregs) in cerebral malaria’s disease progression. Th17 cells, known for their pro-inflammatory activity, become dysregulated during malaria infection, contributing to excessive inflammation and brain pathology. Conversely, Tregs, which typically serve as immune suppressors to maintain homeostasis, are dysfunctional or insufficient in controlling inflammation during cerebral malaria. The disruption of this axis results in unchecked immune activation causing neural damage and clinical deterioration.

Mesenchymal stem cells, derived from bone marrow or other tissue sources, exhibit potent immunoregulatory functions, principally by interacting with various immune cells and secreting immunomodulatory cytokines. In the experimental cerebral malaria model, MSC administration was associated with a dramatic amelioration of disease symptoms and reduced mortality, which prompted researchers to decipher the cellular and molecular mechanisms behind this effect. Their findings illuminated that MSCs induce a unique subset of regulatory T cells that simultaneously express RoRγt—a transcription factor typically linked with Th17 cells—and Foxp3, a master regulator of regulatory T cell development and function.

This intriguing population of Tr17 cells appears to embody a functional hybrid capable of both tempering inflammation and promoting immune regulation in cerebral malaria. The induction of these Tr17 cells disrupts the pathological dominance of proinflammatory Th17 cells, restoring balance in the immune milieu within the central nervous system. This balance correction is critical for preventing the blood-brain barrier breakdown, cerebral edema, and microvascular injury that characterize severe cerebral malaria pathology.

Further deepening the impact of these findings is the insight into how MSCs recalibrate the cytokine environment to favor immune homeostasis. MSCs downregulate key proinflammatory cytokines such as IL-17 and IFN-γ while enhancing anti-inflammatory cytokines like IL-10 — a cytokine tethered to immune suppression and tissue protection. This shift creates a microenvironment conducive to the expansion of Tregs and specifically those expressing both transcription factors, marking a profound reshaping of the Th17/Treg axis.

An equally impressive aspect of this research is the detailed exploration of the molecular pathways triggered by MSCs. They showed that these stem cells engage signaling cascades that encourage naive T cells to differentiate into Tr17 cells rather than purely proinflammatory lineages. This finding reveals a sophisticated immunological reprogramming induced by MSCs, offering avenues for therapeutic interventions that can mimic or enhance this effect pharmacologically or via cell therapy.

The translational potential of this study cannot be overstated. The current clinical management of cerebral malaria primarily relies on antimalarial drugs and supportive care, with little to no specific treatment available to counteract immune-mediated brain damage. The MSC-based approach offers a promising adjunct or alternative therapeutics that could drastically reduce mortality and long-term neurological impairment. Given the global burden of malaria, especially in low-resource settings, the possibility of stem cell therapies or MSC-derived products representing a lifesaving intervention is profound.

However, challenges remain before MSC therapy can be routinely applied in clinical settings. As the study authors emphasize, scaling stem cell production, ensuring safety, avoiding potential adverse immune reactions, and devising delivery methods pose significant hurdles. Furthermore, understanding the long-term effects of inducing Tr17 cells and the precise regulatory mechanisms at the epigenetic and proteomic levels remains an open endeavor for future research.

This research also sparks an exciting discussion about the plasticity and heterogeneity of regulatory T cell subsets. The discovery of the Tr17 phenotype enriches our comprehension of immune regulation in infectious diseases, suggesting that Tregs are not a uniform population but rather a spectrum of niche cells adapted to specific pathological contexts. Unlocking the spectrum of Treg identities may have far-reaching implications beyond malaria, potentially informing immune modulation in autoimmune diseases, cancer, and transplant biology.

The immunological finesse demonstrated by MSCs in orchestrating a favorable immune response hints at a broader renaissance in cell-based therapies. This approach transcends merely suppressing inflammation; instead, it carefully restores immune equilibrium, thus offering targeted and dynamic control over complex immune landscapes. The findings highlight how a deeper mechanistic understanding can guide the pragmatic design of next-generation biologics tailored to the subtleties of immune dysfunction.

Importantly, this study integrates advanced immunophenotyping, molecular biology, and in vivo disease modeling to provide robust evidence for the therapeutic potential of MSCs. It stands as a testament to the power of interdisciplinary collaboration, marrying stem cell biology with infectious disease immunology to tackle one of the most recalcitrant challenges in tropical medicine.

Looking ahead, the possibilities opened up by the discovery of MSC-induced Tr17 cells invite a cascade of investigations to refine and optimize this therapy. Questions about optimal timing of administration, dose responses, interactions with conventional treatments, and effects in human subjects are compelling avenues for clinical trials. Moreover, further dissection of signaling pathways involved in Tr17 cell induction may yield novel drug targets that could substitute for or synergize with cell therapy approaches.

As the global health community continues to wage war against malaria, innovations such as this offer renewed hope. By harnessing the body’s own regulatory machinery through MSCs, scientists have taken a significant step toward transforming the therapeutic landscape of cerebral malaria—a historically devastating disease. This study not only elevates our understanding of malaria immunopathogenesis but sets a blueprint for emerging treatments that blend stem cell science with targeted immune modulation.

In sum, the revelation that mesenchymal stem cells can alleviate cerebral malaria severity by inducing RoRγt⁺ Foxp3⁺ T regulatory cells marks a watershed moment in infectious disease research. It challenges existing paradigms of immune intervention and propels the field toward a future where cell-based therapies could emerge as frontline defenses against deadly infections that have long plagued humanity. The full clinical translation remains on the horizon, but the promise illuminated by this research shines brightly as a beacon of hope against cerebral malaria’s devastating toll.

Subject of Research: The immunomodulatory effect of mesenchymal stem cells on experimental cerebral malaria with a focus on the induction of RoRγt⁺ Foxp3⁺ regulatory T cells and modulation of the Th17/Treg axis.

Article Title: Mesenchymal stem cells alleviate experimental cerebral malaria disease severity by inducing RoRγt⁺ Foxp3⁺ T regulatory (Tr17) cells and modulating the dysregulated Th17/Treg axis.

Article References:
Sharma, I., Thakur, R.S., Chaudhary, A. et al. Mesenchymal stem cells alleviate experimental cerebral malaria disease severity by inducing RoRγt⁺ Foxp3⁺ T regulatory (Tr 17) cells and modulating the dysregulated Th17/Treg axis. Cell Death Discov. (2026). https://doi.org/10.1038/s41420-025-02900-3

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DOI: https://doi.org/10.1038/s41420-025-02900-3

Plasmodium vivax, a parasite responsible for a predominant share of malaria cases outside sub-Saharan Africa, has long challenged scientists due to its complex lifecycle and notorious ability to evade the human immune system. Unlike Plasmodium falciparum, which has been the main focus of malaria research, P. vivax can form dormant liver stages called hypnozoites. These hypnozoites cause relapses weeks to months after an initial infection, complicating treatment and control efforts. Understanding how humans naturally develop immunity to this parasite has remained an unresolved frontier until now.

The study employed a novel approach by administering repeated, controlled infections of P. vivax in volunteers under strict clinical supervision. This controlled human malaria infection (CHMI) model allowed researchers to monitor immune responses with an unprecedented level of granularity, observing how clinical immunity might develop over multiple sequential exposures. Volunteers were carefully screened and treated to ensure safety, highlighting the ethical rigor and innovative design of the human challenge model.

Throughout several infection cycles, researchers meticulously tracked a spectrum of immunological markers, clinical symptoms, and parasitemia levels. The data revealed a gradual acquisition of clinical immunity, characterized by a reduction in symptom severity and parasite loads despite sustained exposure. This phenomenon indicates that the human immune system can adapt and mount increasingly effective defense mechanisms against P. vivax after repeated encounters, challenging the long-held assumption that immunity to this parasite is weak or non-sterilizing.

One of the key breakthroughs reported was the identification of specific immunoprofiles correlating with protective immunity. These profiles include enhanced antibody responses against P. vivax merozoite surface proteins and robust activation of both cellular and humoral immune arms. Furthermore, the study uncovered evidence of immune memory formation, suggesting that repeated infections stimulate long-lasting protection mechanisms, which could be harnessed in vaccine development.

Another remarkable aspect of the research is the demonstration that clinical immunity does not necessarily require complete parasite clearance. Instead, the immune system achieves a state of equilibrium, tolerating low-level parasitemia while preventing symptomatic disease. This finding echoes observations in endemic populations where individuals often harbor asymptomatic infections, reflecting a clinical tolerance rather than absolute immunity. Understanding this balance is crucial for devising strategies that aim to reduce morbidity without necessarily eradicating every parasite.

The implications for vaccine research are profound. Current P. vivax vaccine candidates have struggled to elicit robust and durable immunity partly because of limited knowledge about protective immune correlates. By delineating the immune signatures associated with clinical immunity in this CHMI model, the study offers a valuable template for evaluating and optimizing vaccine candidates. It provides a mechanistic roadmap that could enhance the efficacy of next-generation vaccines targeting critical parasite antigens.

Moreover, the study sheds light on the potential of controlled repeated exposure as a form of immunization. This concept, reminiscent of “leaky” vaccination strategies observed in other infectious diseases, opens intriguing avenues for malaria control. While ethical and logistical challenges limit the broad application of deliberate infection, understanding the principles underlying exposure-mediated immunity may guide innovative immunotherapeutic approaches that mimic natural infection processes.

Technical sophistication in parasite quantification and immune profiling played a pivotal role in this research. The team utilized state-of-the-art quantitative PCR assays to detect parasitemia at ultra-low levels, coupled with advanced flow cytometry and multiplex immunoassays to dissect immune cell populations and cytokine milieus. These cutting-edge methodologies ensured precise measurement of how immune dynamics evolve over successive P. vivax exposures, providing a holistic view of infection-immunity interplay.

Importantly, the study also satisfied stringent safety criteria throughout its conduct. Volunteers were monitored intensively, receiving prompt antimalarial treatment upon parasitemia detection to preclude severe illness. These safety measures underscore the feasibility and ethical soundness of controlled human malaria infection models when executed with diligence, raising prospects for their expanded use in studying other challenging pathogens.

This research contributes significant empirical data to the ongoing debate on why natural immunity to P. vivax is slower to develop compared to P. falciparum. By controlling variables such as infection dose and timing, the study isolates host immune responses from confounding factors typical in endemic field studies, including reinfection heterogeneity and co-infections. Hence, the findings provide cleaner mechanistic insights that reinforce the concept of clinical immunity as a gradual and adaptable process.

Furthermore, the study’s implications extend beyond immunology to public health policy. As malaria elimination programs grapple with the complex transmission dynamics of P. vivax, understanding immunity development will inform surveillance and treatment strategies. Especially in regions where relapse infections perpetuate transmission, interventions leveraging immunity could complement vector control and chemotherapeutic measures to achieve sustainable malaria reduction goals.

Looking ahead, the researchers emphasize the need for expanded studies involving diverse populations, genetic backgrounds, and age groups to capture the full spectrum of immune responses to P. vivax. Since natural immunity is known to vary substantially, understanding the contributions of host genetics and environmental factors remains a priority. Integrating CHMI findings with observational cohort data in endemic areas could offer holistic insights into malaria immunity.

Additionally, the molecular underpinnings of immune evasion by P. vivax parasites warrant further investigation. The parasite’s ability to alter antigen expression, form dormant stages, and modulate host immune pathways continues to challenge eradication efforts. The novel immunological insights generated herein provide a framework for dissecting these evasion mechanisms and identifying vulnerabilities amenable to targeted intervention.

In conclusion, this transformative study marks a watershed moment in malaria research by revealing how sequential controlled infections foster clinical immunity to Plasmodium vivax. The integration of advanced molecular tools, careful clinical design, and immunological analysis has yielded a rich compendium of findings with far-reaching implications. Beyond advancing scientific knowledge, these discoveries kindle hope for more effective vaccines, improved therapeutic regimes, and ultimately, decreased global malaria burden.

As the global health community intensifies efforts to combat malaria, particularly in the context of rising drug resistance and shifting epidemiology, harnessing the natural development of clinical immunity represents a promising frontier. The insights from this study not only challenge existing paradigms but also serve as a clarion call to prioritize translational research that bridges bench discoveries with field applications, accelerating the path toward malaria elimination.

Subject of Research: Development of clinical immunity to Plasmodium vivax through repeat controlled human malaria infection.

Article Title: Development of clinical immunity to Plasmodium vivax following repeat controlled human malaria infection.

Article References:
Hou, M.M., Harding, A.C., Barber, N.M. et al. Development of clinical immunity to Plasmodium vivax following repeat controlled human malaria infection. Nat Commun 16, 8385 (2025). https://doi.org/10.1038/s41467-025-63104-y

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Malaria, caused by Plasmodium parasites, remains one of the world’s deadliest infectious diseases, with pre-erythrocytic stages—the initial phase following parasite entry into the liver—being a critical target for intervention. Despite intense efforts to harness the immune system’s potential to eliminate these liver-stage parasites, efficacy in humans has been variable. This new study deepens our mechanistic comprehension by identifying androgens as key modulators that inhibit cytotoxic CD8⁺ T cell responses, crucial players in clearing infected hepatocytes before parasites can multiply and invade red blood cells.

The research team led by Duncombe, Sen, and Watson employed sophisticated mouse models genetically engineered to illuminate immune interactions with Plasmodium species. Through a series of well-controlled experiments, they demonstrated that increased androgen levels corresponded with a marked decrease in the activation and proliferation of CD8⁺ T cells capable of recognizing infected liver cells. This hormonal regulation bluntly impairs the immune system’s capacity to mount an effective pre-erythrocytic response, thus providing a permissive environment for parasite development and subsequent blood-stage infection.

Delving into the molecular pathways, the researchers found that androgens engage specific androgen receptors expressed on CD8⁺ T cells, initiating a cascade of intracellular signals that antagonize their cytotoxic function. Notably, androgen receptor signaling suppresses crucial transcription factors and cytokine production necessary for T cell activation and memory formation. This crosstalk between steroid hormones and immune cell machinery reveals an unexpected endocrine-immune axis that can be exploited by the parasite to evade early immune clearance.

The implications of these findings extend beyond basic immunology. Given that males generally experience different malaria infection patterns compared to females, this androgen-mediated immunosuppression provides a plausible biological rationale for sex-specific disparities observed in malaria susceptibility and severity. The study’s revelation prompts a reevaluation of how host hormonal status should be considered when designing and testing next-generation malaria vaccines, many of which rely heavily on eliciting durable CD8⁺ T cell responses.

Importantly, the study highlights that androgen deprivation, either via surgical castration or pharmacological inhibition, restores protective CD8⁺ T cell responses in murine models. Such interventions significantly reduce liver parasite load and delay or prevent progression to blood-stage infection. These preclinical findings open the door to novel adjunctive therapies that modulate hormonal milieu to boost vaccine efficacy or enhance natural immunity, especially in populations where traditional vaccine strategies have faltered.

Moreover, the investigation sheds light on intricate immune evasion tactics employed by Plasmodium parasites. By leveraging the host’s own hormones, parasites indirectly dampen immune pressure during the most vulnerable phase of their lifecycle. This sophisticated interplay emphasizes the necessity of integrative approaches in infectious disease research, considering not only the pathogen and the immune system but also the host’s endocrine environment.

From a translational perspective, understanding androgen effects on CD8⁺ T cell dynamics could influence clinical management of malaria in endemic regions. Personalized medicine approaches may incorporate hormonal profiling to identify individuals at heightened risk of severe disease or poor vaccine responsiveness. Additionally, clinical trials might consider stratification by sex and hormonal status to optimize therapeutic outcomes.

Technical examination of the CD8⁺ T cell subsets revealed that androgens predominantly affect effector and memory precursor populations, thereby jeopardizing long-term protective immunity. This disruption compromises the establishment of immunological memory necessary for sustained protection upon reinfection, a major challenge in malaria vaccine development. The suppression of critical cytokines such as IFN-γ and TNF-α further undermines the cytotoxic arsenal of these T cells.

The study also used transcriptomic analyses to trace the androgen-induced molecular signature within CD8⁺ T cells, identifying down-regulation of genes involved in T cell receptor signaling and metabolic pathways essential for cell proliferation and survival. These findings suggest that androgen signaling reprograms T cells into a less responsive state, hampering their ability to eradicate parasite-infected hepatocytes effectively.

This research is notable for integrating immunology, endocrinology, and parasitology, forging new avenues for multidisciplinary collaboration in combating malaria. Future studies might explore how fluctuations in androgen levels across different life stages and physiological conditions influence malaria immunity. Such insights could guide targeted interventions during periods of heightened susceptibility, such as puberty or androgen therapy in clinical scenarios.

Furthermore, the interplay between androgen signaling and other immune-modulatory pathways remains an exciting frontier. Investigating synergistic or antagonistic effects between hormones, cytokines, and pathogen-derived molecules could unveil novel checkpoints of immune regulation. Understanding these complex networks will be vital for designing interventions that circumvent the immune dampening effects induced by androgens.

In summary, Duncombe and colleagues’ study profoundly alters the paradigm of malaria immunology by identifying androgens as inhibitors of protective CD8⁺ T cell responses during the critical pre-erythrocytic stage. This discovery lays a foundation for innovative therapeutic strategies that harness hormonal modulation to enhance immune clearance of malaria parasites before they can establish systemic infection. The work promises to accelerate the quest for more effective malaria vaccines and treatments tailored to the host’s endocrine makeup.

As the global health community intensifies efforts to eradicate malaria, findings such as these underscore the complexity of host-pathogen interactions and the necessity of considering host biology beyond traditional immunological parameters. By illuminating the suppressive role of androgens on essential immune responses, this study invites a rethinking of how sex hormones shape infectious disease outcomes and potentially offers a transformative angle for intervention in the fight against one of humanity’s oldest scourges.

Subject of Research: The influence of androgens on CD8⁺ T cell-mediated immune responses against pre-erythrocytic stages of malaria parasites in mice.

Article Title: Androgens inhibit protective CD8⁺ T cell responses against pre-erythrocytic malaria parasites in mice.

Article References:
Duncombe, C.J., Sen, N., Watson, F.N. et al. Androgens inhibit protective CD8⁺ T cell responses against pre-erythrocytic malaria parasites in mice. Nat Commun 16, 5172 (2025). https://doi.org/10.1038/s41467-025-60193-7

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For decades, scientists have recognized that P. falciparum escapes immune clearance through the sophisticated regulation of its var gene family, which encodes the critical virulence factor PfEMP1. PfEMP1 molecules are displayed on the surface of infected red blood cells and serve as both the parasite’s primary interface with host tissues and a key target of immune responses. The process of transcriptional switching between distinct var genes effectively changes the molecular “face” of the parasite, enabling it to dodge antibodies tuned to previous variants. The prevailing view held that within any individual parasite, a strict monoallelic expression ensured a single var gene dominated the surface antigen repertoire at a time, maintaining antigenic coherence and immune evasion.

However, the new study by Florini et al. employs single-cell RNA sequencing (scRNA-seq) augmented by the novel use of targeted enrichment probes and microfluidic systems to survey var gene expression at an unprecedented resolution. Unlike earlier bulk RNA approaches that masked cellular heterogeneity, this single-cell approach uncovers a remarkable transcriptional plasticity in var gene regulation within clonal populations of both 3D7 and IT4 laboratory strains. Intriguingly, rather than displaying strict monoallelic expression, individual parasites were found to express multiple var genes concurrently, or alternatively enter states featuring minimal to undetectable var transcription.

This discovery upends a fundamental assumption in malaria biology. The presence of multiple var transcripts per cell implies a more complex mechanism of antigenic variation than previously postulated. It suggests that parasites can not only switch between surface antigens but might transiently present multi-variant repertoires or effectively “turn down” their antigenic profile altogether, thereby modulating their immunological visibility. The existence of parasite subpopulations with diminished PfEMP1 expression correlates with notably reduced recognition by host antibodies, effectively rendering these parasites antigenically invisible.

To elucidate these dynamics, the researchers developed a bespoke framework combining targeted enrichment of var transcripts with a portable microwell platform optimized for capturing the rare and variable transcripts at single-cell resolution. This technological innovation allowed them to parse the intricate expression patterns that define parasite populations, revealing transcriptional heterogeneity within clones previously assumed to be uniform. The data showed that parasites can adopt three distinct transcriptional states: monoallelic var expression, simultaneous co-expression of several var genes, and a silenced var state characterized by minimal expression.

The biological implications are profound. The co-expression of multiple var genes potentially offers a window into intermediate states during transcriptional switching or a strategy to diversify antigenic presentation within a single parasite, complicating the immune system’s task of mounting an effective response. Conversely, the silenced var state suggests a dormant-like or immune-evasive form that may underpin chronic asymptomatic infections, where parasites persist under the radar of host immunity for extended periods.

Such plasticity in var gene regulation aligns with clinical observations where chronic malaria infections often display low parasite densities and subdued immune activation. These asymptomatic carriers serve as reservoirs for transmission and present a significant obstacle to malaria elimination efforts. By showing that transcriptional flexibility can generate “invisible” parasites, this study provides a mechanistic framework for understanding how the malaria parasite can persist undetected, sustaining transmission cycles in endemic regions.

The work also invites reconsideration of vaccine design strategies that target PfEMP1 or its variants. If parasites can simultaneously produce multiple PfEMP1 variants or suppress their surface antigen expression, vaccines aimed at single or limited antigens may falter. A more nuanced approach, perhaps combining multi-epitope formulations or strategies that disrupt the regulatory machinery governing var transcription, could be warranted. Additionally, therapies that force parasites out of their “silent” state could expose them to immune clearance.

From a technical standpoint, the study exemplifies the power of single-cell transcriptomics to revolutionize host-pathogen biology. Traditional bulk RNA analyses average signals from millions of cells, masking rare transcriptional states that may be critical for pathogen survival. By contrast, this single-cell methodology reveals cell-to-cell variability, uncovering hidden phenotypic states and providing a rich landscape of regulatory mechanisms. The deployment of targeted enrichment probes further sharpened this resolution, enriching low-abundance var transcripts that are otherwise difficult to detect.

Moreover, the researchers’ use of clonal parasite lines ensured that transcriptional heterogeneity arose from gene regulation rather than genetic diversity, highlighting epigenetic and transcriptional feedback loops as drivers of this plasticity. These findings dovetail with emerging evidence of chromatin remodeling and nuclear organization playing pivotal roles in var gene regulation, implicating multiple layers of control in shaping antigenic diversity.

Understanding this transcriptional plasticity also raises new questions about the molecular signals and environmental cues that transition parasites between the three identified var expression states. It opens avenues to explore how host immune pressure, red blood cell physiology, or metabolic factors may influence these transitions. Deciphering these regulatory inputs could identify vulnerability points to disrupt parasite survival strategies.

The discovery further impacts our comprehension of parasite population dynamics within hosts. Rather than viewing infected red blood cell populations as antigenically homogenous, this work reveals a mosaic of expression states at any given time. Such heterogeneity may facilitate niche partitioning, immune evasion on multiple fronts, and robust survival amidst fluctuating host defenses. It could also contribute to the parasite’s ability to adapt rapidly to new host environments or therapeutic pressures.

In summary, the study by Florini et al. breaks new ground by demonstrating that Plasmodium falciparum’s var gene expression is far from the simplistic monoallelic model once assumed. Instead, individual parasites display a surprising transcriptional plasticity that toggles between multiple gene expression profiles and silent states. This flexibility equips the parasite with a sophisticated toolkit to modulate antigenic presentation, evade host antibodies, and sustain chronic infections that silently fuel malaria transmission worldwide.

As the malaria research community digests these findings, incorporating this newfound complexity into models of parasite biology and immune interaction will be crucial. It challenges researchers to rethink vaccine and therapeutic design, guiding efforts to target the parasite’s regulatory circuits controlling var gene expression. Ultimately, this advance highlights how technological innovation in single-cell genomics can unravel the hidden strategies pathogens use to outwit immunity, inspiring new routes to combat one of humanity’s deadliest foes.

Subject of Research: Mechanisms of var gene expression regulation in Plasmodium falciparum and its role in immune evasion.

Article Title: scRNA-seq reveals transcriptional plasticity of var gene expression in Plasmodium falciparum for host immune avoidance.

Article References:
Florini, F., Visone, J.E., Hadjimichael, E. et al. scRNA-seq reveals transcriptional plasticity of var gene expression in Plasmodium falciparum for host immune avoidance. Nat Microbiol (2025). https://doi.org/10.1038/s41564-025-02008-5

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