Welcome to KodaKoda's Weekly Immunology News. I'm so glad you're joining us today because this week is absolutely packed with fascinating science. We have stories about gene therapy for deafness, bacterial immune systems that fight viruses, a potential new approach to vaccines, and much more. Let us dive right in.
First up, we are talking about something that sits right at the intersection of gene therapy and immunology. The study is titled Re-administration of AAV-mediated gene therapy for OTOF-related deafness a single-arm trial, published in Nature Medicine on June 26th, 2026. The first author is Xintai Fan from the ENT Institute and Department of Otorhinolaryngology at the Eye and ENT Hospital of Fudan University in Shanghai, China.
So here is the challenge this study is tackling. When you give someone a gene therapy using a delivery vehicle called an adeno-associated virus, or AAV for short, the body often mounts an immune response and produces what are called neutralizing antibodies. Those antibodies remember the AAV and can block future doses from working. That is a real problem if a patient needs treatment in both ears, for example. This study looked at individuals with OTOF-related deafness, which is a form of congenital hearing loss caused by mutations in the otoferlin gene. The researchers had previously shown that a single dose of AAV carrying a healthy copy of the gene was safe and improved hearing.
Now they wanted to know what happens when you give a second dose to the other ear, especially in patients who already have those neutralizing antibodies circulating in their blood. They first tested this in mice that had very high levels of neutralizing antibodies, and the re-administration successfully rescued hearing with only limited immune activation. That was encouraging enough to move forward in humans. Four young patients between two and a half and three and a half years old, all with pre-existing neutralizing antibodies at varying levels, received a second dose in their untreated ear. They were followed for anywhere between 26 and 52 weeks. The primary thing they were watching for was dose-limiting toxicities at six weeks, and none occurred. In terms of hearing, the results were meaningful. The average brainstem response threshold in the newly treated ear, which is a measure of how loud a sound needs to be before the brain registers it, improved dramatically from greater than 95 decibels at baseline to between 43 and 80 decibels across the four patients. All adverse events were mild to moderate, grade 1 or 2, except for one case of a grade 3 decrease in neutrophil count, which are immune cells involved in fighting infection, but no serious adverse events occurred overall. The researchers conclude that while these findings are preliminary and larger studies are needed, they offer real hope that re-administration of AAV gene therapy across ears can be done safely even in the presence of pre-existing immunity.
Now let us move into microbiology, and this is a really cool one for anyone who is fascinated by the microscopic arms race between bacteria and the viruses that attack them, which we call bacteriophages or just phages. The paper is titled END nucleases are antiphage defence systems targeting multiple phages with modified genomes, published in Nature Microbiology on June 26th, 2026. The first author is Wearn-Xin Yee from the Department of Microbiology and Immunology at the University of California, San Francisco.
So bacteria have evolved all kinds of immune strategies to protect themselves from phages, and these systems tend to cluster together in regions of the bacterial genome called defence islands. The researchers here were studying a Pseudomonas aeruginosa strain isolated from a cystic fibrosis patient. Pseudomonas aeruginosa is a particularly troublesome pathogen, and phages from a group called the Pbunavirus family are actually being explored as phage therapies to treat these infections. The team identified a single gene in a defence island that was responsible for blocking those phages from infecting the bacterium. They named the resulting defence system END nucleases, which is a newly described type of defence mechanism. What makes it special is its structure. It has a domain similar to a Type IIS restriction endonuclease, which is basically a molecular scissors that cuts DNA at specific sequences, fused to another domain that is catalytically inactive but normally functions to recognize non-canonical or unusual bases in DNA. Together, this combination allows END nucleases to target phages that have chemically modified DNA in their genomes. And here is what is remarkable. The system is not picky about which modification it detects. It can recognize and attack phages from up to eight different families that use at least ten different types of known DNA modifications beyond simple methylation. Think of it like a broad-spectrum immune sensor for unusual DNA. The researchers also found that the phages themselves fight back. Phages from the Pbunavirus and Wroclawvirus families encode proteins that directly bind to and inhibit END nucleases. This kind of co-evolutionary arms race is what makes microbial immunology so endlessly fascinating.
Staying in the world of bacterial immunity, our next paper is titled Potential role of a CRISPR-Cas-activated toxin-antitoxin system in bacterial immunity, published in Nature Communications on June 26th, 2026, with first author Jiyun Chen from the State Key Laboratory of Cellular Stress Biology at Xiamen University in China.
Most people have heard of CRISPR-Cas systems as genome editing tools, but in nature they evolved as bacterial immune systems to fend off phages. Separately, bacteria also use toxin-antitoxin systems, where a toxic protein is kept in check by an antitoxin, and under certain conditions, like phage infection, the toxin can be released to slow down cellular processes and limit phage spread. This paper looks at whether these two distinct immune strategies can work together synergistically. The researchers studied a CRISPR-Cas13a system and a type II toxin-antitoxin module called HicAB from a bacterium called Leptotrichia. They expressed these systems in E. coli and performed detailed biochemical and structural analyses. What they found was genuinely surprising. The antitoxin, HicB, which you might expect to simply neutralize the toxin, actually has its own toxic properties when directly activated by Cas13a. So Cas13a, upon sensing phage infection, directly activates HicB, which then triggers growth inhibition and protects against bacteriophages. The toxin HicA can compete for binding to HicB and thereby block Cas13a from activating it, which adds another layer of regulatory complexity. Even more elegantly, the CRISPR RNA itself forms a large complex with HicAB that physically blocks HicA's active site, neutralizing its toxic function and keeping the system in balance under normal conditions. The study reveals a beautifully complex functional synergy between two distinct bacterial immune strategies, and it raises new questions about how widespread this kind of cooperation might be across the microbial world.
Next we are heading into the world of fungal infections and the vaginal microbiome. The paper is titled Saccharomyces cerevisiae reduces vulvovaginal candidiasis severity through modulation of fungal pathogenicity and inflammatory responses, published in Nature Communications on June 26th, 2026. The first author is Mart Sillen from the Laboratory of Molecular Cell Biology at KU Leuven in Belgium.
Vulvovaginal candidiasis, or VVC, is an incredibly common infection caused predominantly by Candida albicans. Millions of women experience it every year, and the disease involves a complicated interplay between fungal virulence, epithelial tissue damage, and immune dysfunction, particularly involving neutrophils, which are the frontline immune cells that rush to sites of infection. The problem in VVC is that neutrophils become hyperactivated and dysfunctional, contributing to tissue damage rather than resolving the infection. The researchers explored whether a different yeast, Saccharomyces cerevisiae, the same species used in baking and brewing, could be used as a live biotherapeutic to treat VVC. They identified a specific isolate they called Sc3458 and tested its effects on Candida albicans virulence and host immune responses. The results were striking. Sc3458 impaired Candida albicans in multiple ways, it reduced fungal proliferation, inhibited adhesion to surfaces, and blocked the transition from a yeast form to the more invasive hyphal form, all of which are key to Candida's ability to form biofilms and cause disease. At the molecular level, this was accompanied by transcriptional reprogramming in the pathogen, with downregulation of genes involved in virulence and biofilm formation and signs of metabolic stress. On the immune side, Sc3458 dampened inflammatory responses and reduced neutrophil hyperactivation while preserving the ability of neutrophils to still kill the fungus when needed. In a mouse model of VVC, these combined effects translated to better infection control and reduced hyperinflammation. The authors are optimistic that Sc3458 could be a promising candidate for a live biotherapeutic but note that clinical validation in humans will be essential.
Our next story involves one of the most ambitious frontiers in transplantation medicine: using pig organs in humans. The paper is titled Multiple human transgenes prolong survival of triple-carbohydrate knockout porcine kidney xenografts in nonhuman primates, published in Nature Communications on June 27th, 2026. The first author is Ahmad Karadagi from the Center for Transplantation Sciences at Massachusetts General Hospital and Harvard Medical School in Boston.
There is a massive global shortage of donor organs, and genetically modified pigs are being developed as a potential solution. The main immunological barrier is that pig cells express specific sugar molecules on their surface called carbohydrate xenoantigens, and the human immune system immediately recognizes these as foreign and attacks the transplanted organ. Scientists have created pigs that lack the three major carbohydrate xenoantigens, called triple-knockout or 3KO pigs. But even without those sugars, there are still protein incompatibilities between pig and human biology that can trigger immune rejection. This study looked at which combinations of human transgenes, meaning human genes inserted into the pig genome, work best to overcome those protein incompatibilities. They tested four different combinations of human transgenes in kidney xenografts, using a nonhuman primate model, and measured immune responses and transplant survival. The addition of human transgenes significantly reduced the molecular signals of early immune activation, leading to markedly prolonged survival of the transplanted kidneys. Particularly interesting was the finding that including the anti-inflammatory genes TNFAIP3 and HMOX1 was associated with improved graft survival, reduced infiltration by T cells and a type of myeloid immune cell marked by a surface protein called CD11b, and lower expression of rejection-related gene sets in tissue biopsies from the transplanted organs. This is the kind of incremental but important progress that is steadily bringing xenotransplantation closer to clinical reality.
Now this next paper is going to get vaccine enthusiasts very excited. It is titled Multiomic analysis identifies glutaminolysis-dependent metabolic enhancement of immune memory utilised for vaccine development, published in Nature Communications on June 26th, 2026. The first author is J M Sowerby from the Cambridge Institute of Therapeutic Immunology and Infectious Disease in Cambridge, UK.
One of the great challenges in vaccinology is inducing strong, long-lasting immune memory, especially in vulnerable groups like the elderly whose immune systems do not respond as robustly to vaccines. This study took a clever approach: they screened the transcriptional signatures of T cell memory against databases of drug signatures to identify existing approved drugs that might promote a memory precursor phenotype in T cells. They honed in on a class of compounds called lysine deacetylase inhibitors, or KDACi for short. These are drugs that affect gene expression by modifying how DNA is packaged and accessible. Using a remarkable multimodal approach combining acetylomic, metabolomic, transcriptomic, and epigenomic analyses, the researchers pinpointed the mechanism. KDACi promote immune memory by enhancing a metabolic pathway called glutaminolysis, which is the cellular process of breaking down the amino acid glutamine for energy and biosynthesis. Selectively blocking glutaminolysis reversed the memory-promoting effects of KDACi treatment, confirming this is the key mechanism. They validated these findings in four different mouse models of infection and immunization. Then came the headline result. They conducted a human challenge study using a repurposable KDACi called sodium valproate, which is actually an existing epilepsy and mood disorder medication, and combined it with seasonal influenza vaccination. The result was a ten-fold increase in correlates of protection in vaccinated individuals. That is a remarkable finding that suggests we may be able to dramatically boost vaccine effectiveness using already-approved medications by targeting the metabolic state of memory T cells.
Let us stay with bacterial immunity and move to a paper about a specific immune system called Kongming, which was named after the famous Chinese strategist Zhuge Kongming, fitting given how clever and elaborate this defense mechanism turns out to be. The paper is titled dITP-induced remodeling activates the filamentous effector complex in Kongming anti-phage defense, published in Nature Communications on June 26th, 2026. The first author is Xia Li from the Hubei Key Laboratory of Industrial Biotechnology at Hubei University in Wuhan, China.
The Kongming system is a bacterial anti-phage immune system that works through nucleotide signaling. It has an effector complex called KomBC, made up of two proteins: KomB, which is a non-canonical purine NTP pyrophosphatase, and KomC, which contains a domain called SIR2 that has NADase activity, meaning it can break down NAD, an essential molecule for cellular metabolism. When a phage infects a bacterium, the Kongming system generates an unusual signaling nucleotide called dITP. The question this paper addresses is how exactly dITP activates the KomBC complex to cause the bacterium to deploy its defense. Through detailed structural and functional analyses, the researchers found that KomBC assembles into a helical filament made up of stacked repeating units of four KomB proteins and four KomC proteins. When dITP binds to KomB, it triggers a cascade of conformational changes, essentially rearranging the shape of the filament into a new architecture where KomC transitions into an active state and can now perform its NADase activity, depleting NAD and disrupting cellular metabolism in a way that halts phage replication. The study also identifies a key amino acid residue in the SIR2 domain that appears to be important for this NADase activation, which may have broader implications for understanding how SIR2 family proteins work across different bacterial immune systems.
Now let us shift to human autoimmune disease. This next paper uses cutting-edge spatial transcriptomics to map the immune landscape of skin in a condition called dermatomyositis. The paper is titled Spatial transcriptomics identifies immune-stromal niches associated with cancer in adult dermatomyositis, published in Nature Communications on June 26th, 2026. The first author is Ksenia Anufrieva from the Division of Rheumatology, Inflammation, and Immunity at Brigham and Women's Hospital, Harvard Medical School in Boston.
Dermatomyositis is a rare autoimmune inflammatory disease that affects muscles and causes distinctive skin rashes. One of its most clinically important features is a strong association with malignancy, meaning some patients have dermatomyositis because they have an underlying cancer and the immune system is responding abnormally. This study used spatial and single-cell transcriptomics to map exactly which immune and stromal cells are present in the skin lesions of dermatomyositis patients, and compared them to patients with cutaneous lupus erythematosus, another inflammatory skin disease, to identify what is unique to dermatomyositis. The results were very informative. In dermatomyositis patients who had underlying cancer, the skin lesions contained either dispersed immune infiltrates enriched with macrophages or organized lymphoid aggregates with dense cores of B cells surrounded by both CD4-positive and CD8-positive T cells, with preserved vascular architecture. In contrast, dermatomyositis patients without cancer had very different skin lesions characterized by dense myeloid cell infiltrates with elevated expression of the inflammatory cytokines IL-1 beta and CXCL10 near damaged blood vessel walls. Those cytokines, produced by myeloid cells in the context of local tissue hypoxia, drove dramatic stromal remodeling and loss of vascular-associated fibroblasts. Non-cancer-associated dermatomyositis was also characterized by specific cellular partnerships: PD-L1-expressing mature dendritic cells enriched in immunoregulatory molecules, and activated regulatory T cells expressing NFKB2 and TNF receptors. While both dermatomyositis and cutaneous lupus showed strong interferon signatures, dermatomyositis uniquely displayed expression of IFN-beta specifically. This kind of detailed spatial immune mapping helps us understand why dermatomyositis behaves so differently depending on whether cancer is the underlying driver.
Now here is a story that might surprise some listeners because it connects gut bacteria to Alzheimer's disease. The paper is titled Gut bacterial metabolite imidazole propionate potentiates Alzheimer's disease pathology, published in Nature Communications on June 26th, 2026. The first author is Vaibhav Vemuganti from the Department of Bacteriology at the University of Wisconsin-Madison.
The gut microbiome has been increasingly linked to brain health, but the specific mechanisms are often unclear. This study focused on a bacterial metabolite called imidazole propionate, or ImP, which is produced by certain gut bacteria from the amino acid histidine. The researchers found compelling evidence across multiple levels that ImP contributes to Alzheimer's disease and related dementias. In a large cohort of nearly 1200 cognitively unimpaired adults, higher plasma ImP levels were associated with lower scores on preclinical cognitive assessments and worse biomarkers of Alzheimer's and related dementias, both when you look at a single time point and over time. Metagenomic analysis of fecal samples linked the bacteria that produce ImP to Alzheimer's-related phenotypes. A genome-wide integrative analysis then identified a genetic locus on chromosome 12 that is associated with both plasma ImP levels and Alzheimer's disease risk in humans, suggesting that host genetics influences how much ImP a person produces and that this connection is more than just a correlation. In mice, chronic administration of ImP worsened Alzheimer's-like pathology. At the cellular level, ImP impaired the endothelial barrier of blood vessels in the brain, contributing to what is sometimes called leaky brain vasculature, and it promoted the hyperphosphorylation of tau protein in primary neurons, a hallmark of Alzheimer's disease. That tau effect was blocked by inhibiting an enzyme called glycogen synthase kinase-3 beta, pointing to a potential therapeutic target.
Next we have a detailed study of autoantibodies in a rare lung disease. The paper is titled Affinity and epitope-dependent pathogenicity of GM-CSF autoantibodies in patients with autoimmune pulmonary alveolar proteinosis, published in Nature Communications on June 26th, 2026. The first author is Shinji Futami from the Laboratory of Lymphocyte Differentiation at the WPI Immunology Frontier Research Center at the University of Osaka in Japan.
Autoimmune pulmonary alveolar proteinosis, or aPAP, is a rare but serious lung disease where the immune system produces autoantibodies that target a protein called granulocyte-macrophage colony-stimulating factor, or GM-CSF. GM-CSF is critical for the development and function of immune cells called alveolar macrophages, which keep the lungs clean by clearing out debris. When it is blocked by autoantibodies, protein-rich material accumulates in the air sacs of the lungs. One puzzling clinical observation is that the total level of GM-CSF autoantibodies in the blood does not correlate well with how severe the disease is. This study tried to understand why. The researchers characterized 186 monoclonal anti-GM-CSF autoantibodies derived from B cells of 28 aPAP patients with varying disease severity. They classified the antibodies into two groups based on which part of the GM-CSF molecule they bind to, called the epitope. Class 1 antibodies target specific epitopes labeled A, BD, or D, while class 2 antibodies target B or C epitopes. They found that for class 1 antibodies, how tightly the antibody binds to its target, the affinity, strongly predicts its ability to neutralize GM-CSF, whereas for class 2 antibodies that relationship was much weaker. High-affinity class 1 antibodies were found at higher levels in patients with more severe disease, and these antibodies were sufficient on their own to induce PAP symptoms in a humanized mouse model. This elegantly explains why simply measuring total autoantibody levels misses the picture: what matters is the combination of which epitope is being targeted and how strongly the antibody binds.
Now let us talk about one of the greatest ongoing threats in global medicine: antimicrobial resistance. The paper is titled Predicting antimicrobial resistance for precision medicine, published in Cell Host and Microbe on June 26th, 2026. The first author is Theresa Fink from the Institute for Biological Physics at the University of Cologne in Germany.
This is a perspective piece, meaning it is more of a review and forward-looking analysis than a primary research study, but it contains important insights. Antibiotics have been transformative for human health, but bacteria continue to evolve resistance to them, threatening to return us to an era when common infections were deadly. The authors highlight recent progress in using machine learning and artificial intelligence to predict antimicrobial resistance in pathogens based on rapid whole-genome sequencing and other accessible clinical data. Rather than treating all bacterial infections the same way, the vision is a precision medicine approach where you sequence the pathogen quickly, use AI to predict exactly which antibiotics it will be resistant or susceptible to, and choose the most targeted treatment possible. The authors discuss how this approach could also help minimize collateral damage to the patient's microbiome, which is often disrupted by broad-spectrum antibiotic use. They also highlight the potential role of narrow-spectrum therapeutics and adjuvants that could help classical antibiotics work better while slowing the evolution of resistance. This is a helpful map of where the field is heading and what the key scientific and clinical challenges still need to be overcome.
Here is a paper that reveals a completely new mechanism of how the body triggers inflammation in allergic airway disease. The title is Iron drives protease-independent cleavage of gasdermin D in allergic airway diseases, published in Cell on June 26th, 2026. The first author is Shuangfeng Chen from the Key Laboratory of Multi-Cell Systems at the Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences.
Gasdermin D is a protein that plays a major role in a form of inflammatory cell death, and it also functions as a channel in the cell membrane to allow certain signaling molecules to escape the cell. One of those molecules is interleukin-33, or IL-33, which is a potent alarm signal that triggers airway inflammation when the lungs are exposed to allergens. The classical understanding is that gasdermin D is activated by specific proteases, meaning enzymes that cleave it. But this paper reveals an entirely different activation mechanism involving iron. When epithelial cells lining the airways are exposed to allergens, they activate a receptor on their surface called protease-activated receptor 1, or PAR1. This triggers a process called ferritinophagy, in which the cell breaks down its own ferritin, which is the protein that stores iron. This releases what is called labile iron, a free pool of iron inside the cell. A protein called the iron chaperone PCBP2 then delivers this iron directly to gasdermin D. The iron initiates a highly localized chemical reaction called a Fenton reaction, which generates hydroxyl radicals that literally cleave gasdermin D without any protease involved, releasing the active N-terminal fragment that then forms pores in the membrane through which IL-33 escapes to the outside, where it activates group 2 innate lymphoid cells and drives airway inflammation. Blocking any step in this pathway, whether by chelating the iron or genetically removing key components, abolished IL-33 secretion and protected mice from allergic airway inflammation. This is a genuinely surprising mechanistic discovery that opens up new therapeutic avenues for conditions like asthma and allergic lung disease.
Now let us talk about immune function in one of the most serious clinical conditions in intensive care: sepsis. The paper is titled Disturbed metabolic adaptation drives natural killer cell dysfunction in association with nosocomial infection during human sepsis, published in EBioMedicine on June 26th, 2026. The first author is André van der Wurff from the Department of Trauma, Hand, and Reconstructive Surgery at University Hospital Essen in Germany.
Sepsis is a life-threatening organ dysfunction caused by a dysregulated immune response to infection. Patients who survive the initial septic insult are paradoxically at very high risk of developing secondary hospital-acquired, or nosocomial, infections because their immune system becomes suppressed. Natural killer cells, or NK cells, are innate immune cells that are critical first responders to bacterial infection. They release a cytokine called interferon-gamma, or IFN-gamma, which coordinates the killing of pathogens. IL-12 and other cytokines normally stimulate NK cells to ramp up their metabolism, which is required to produce IFN-gamma at scale. The researchers conducted a longitudinal study following NK cells in septic patients over time and found that the expression of the IL-12 receptor and downstream IFN-gamma production in response to Staphylococcus aureus exposure were suppressed for at least 14 days after sepsis diagnosis. This suppression was particularly pronounced in patients who went on to develop secondary infections. Critically, the dysfunction was not caused by the external environment around the NK cells but was cell-intrinsic, meaning something within the NK cells themselves was broken. Mechanistically, the cells showed impaired activation of a major metabolic regulator called mTORC1, which stands for mechanistic target of rapamycin complex 1, and they had reduced expression of nutrient transporters needed for the anabolic metabolism required to sustain IFN-gamma production. Fascinatingly, inhibiting a different metabolic regulator called AMPK, which normally acts as a brake on mTORC1, restored mTORC1 activity and rescued IFN-gamma production in NK cells from septic patients. This points to AMPK inhibition as a potential therapeutic strategy to restore NK cell function and reduce the risk of secondary infections in sepsis patients.
Our next paper comes from a large-scale epidemiological study in England looking at COVID-19 in immunocompromised individuals. The title is Factors associated with severe COVID-19 in immunocompromised subgroups in England from 2020 to 2024 an OpenSAFELY cohort study, published in EBioMedicine on June 26th, 2026. The first author is Edward Parker from the London School of Hygiene and Tropical Medicine.
People with compromised immune systems have been known from the start of the pandemic to be at elevated risk from COVID-19, but the specific factors driving that risk within different immunocompromised subgroups had not been comprehensively studied across successive waves. This study used the OpenSAFELY platform, which is a large-scale secure data analytics platform covering NHS England records, to study five groups: solid organ transplant recipients, people with bone marrow compromise, those on active radio or chemotherapy, those on active immunosuppressive medication, and people with primary or acquired immunodeficiency. They analyzed data across five COVID-19 waves from wave one through the JN.1 omicron subvariant wave. The study included between about 475,000 and 508,000 immunocompromised individuals per wave. Several clear patterns emerged. Solid organ transplant recipients, those with bone marrow compromise, and those on active cancer therapies consistently had the highest rates of severe COVID-19 compared to the other groups. Vaccination within 12 weeks of the start of a wave was consistently associated with reduced risk of severe COVID-19 across all subgroups and all waves, though the effect was somewhat smaller in solid organ transplant recipients, likely because their immunosuppressive medications blunt vaccine responses. Even during the JN.1 wave, vaccination remained protective with adjusted hazard ratios well below 1 for most subgroups. Older age and a higher number of comorbidities were the strongest predictors of severe disease across all groups and all waves. These findings reinforce the importance of prioritizing vaccination and booster doses in immunocompromised populations even as the virus continues to evolve.
And the final paper with an abstract this week comes from a birth cohort study examining early life factors that shape both the gut microbiome and childhood obesity risk. The paper is titled Intrapartum caesarean delivery and childhood BMI trajectories in relation to the infant gut microbiome in the VDAART prospective birth cohort, published in EBioMedicine on June 26th, 2026. The first author is Zheng Sun from the Channing Division of Network Medicine at Brigham and Women's Hospital and Harvard Medical School. The abstract for this paper was cut off before the details of the findings could be shared, but the study is exploring a very important and timely question about how delivery mode, specifically caesarean section, influences the infant gut microbiome and whether those microbiome differences shape a child's body mass index trajectory over time. This is a growing area of research given that both the microbiome in early life and the global childhood obesity epidemic are receiving enormous attention.
Before we wrap up, let us briefly touch on a few other papers that came out this week but without full abstracts available.
In Science Immunology, there was an erratum for a research article titled Claudins interact with LILRB immune inhibitory receptors to promote myeloid immunosuppression in cancer. Errata are corrections to previously published work, and given that Science Immunology is entirely focused on immunology, this touches on the important biology of how cancer evades immune surveillance through myeloid cell suppression.
In Nature Medicine, there is a piece by Karen O'Leary titled HPV vaccination linked to dramatic reduction in cervical cancer deaths. We do not have a full abstract but the headline says it all: further real-world evidence is emerging that human papillomavirus vaccination is saving lives on a large scale by preventing cervical cancer.
There is an author correction in Nature Communications by Wenqi Chen from East China Normal University in Shanghai regarding a paper on how ATF7IP and SETDB1-mediated epigenetic programming regulates thymic homing and T lymphopoiesis of hematopoietic progenitors during embryogenesis, which touches on fundamental developmental immunology.
In Cell, there is a paper by Feng Lin titled Multimodal targeting chimeras enable integrated immunotherapy leveraging tumor-immune microenvironment. Again no abstract available, but the title points to an exciting new approach to cancer immunotherapy using molecules designed to simultaneously engage multiple components of the tumor immune microenvironment.
In Nature, there is an author correction by Ao Guo from the Department of Immunology at St Jude Children's Research Hospital regarding a paper on cBAF complex components and MYC cooperating early in CD8-positive T cell fate. This deals with the molecular machinery that determines how T cells are programmed during development.
Also in Nature, there is an addendum by Carme Riutord from the Helmholtz Institute for One Health in Greifswald, Germany, related to a paper on transmission of MPXV, which is mpox virus, from fire-footed rope squirrels to sooty mangabeys. This contributes to our understanding of how mpox moves between animal species, which is critical for understanding zoonotic spillover risk to humans.
Nature also carried two related pieces on an exciting antibiotic discovery: one news item by Mohana Basu titled Antibiotic cocktail made by soil bacteria can kill superbugs, and an associated article by Steven Rutherford titled Megacluster of genes enables bacteria to make potent antibiotic mixture. These report on a remarkable finding that soil bacteria carry a very large gene cluster that allows them to produce a mixture of antibiotics with potent activity against drug-resistant superbugs, offering potential new leads in the fight against antimicrobial resistance.
In Gastroenterology, there is a brief exchange between research groups. Yajie Wang from Peking University First Hospital published a letter titled Methodological Considerations on Neonatal Metabolomics and Future Inflammatory Bowel Disease, and Jonas Rudbaek from Aalborg University in Copenhagen published a Reply to that letter. These letters discuss methodological nuances in studying early-life metabolites as predictors of inflammatory bowel disease, which is an important area as researchers try to understand why gut immune diseases develop.
And finally, in Nature Immunology, there are two important items. First, there is an author correction by Jing Geng from Xiamen University regarding a paper on how the transcriptional coactivator TAZ regulates the reciprocal differentiation of TH17 cells and regulatory T cells, or Tregs. TH17 and Treg balance is absolutely central to autoimmunity and inflammation, so this is important foundational work. Second and this one has people in the immunotherapy world talking, there is a paper by Adeleye Adeshaki titled Costimulation drives CAR-T cell division fate. CAR-T cell therapy is the revolutionary approach of engineering a patient's own T cells to attack cancer, and understanding what determines how those engineered cells divide and persist is crucial for improving therapy outcomes. This is published in Nature Immunology, which covers exclusively immunology research at the highest level, and we will be keeping an eye out for the full details.
That is everything we have for you this week on KodaKoda's Weekly Immunology News. What a week it has been, from gene therapy and bacterial immune systems to vaccine adjuvants, Alzheimer's disease, and the latest in cancer immunotherapy. The science of immunity never stops moving forward. Thank you so much for listening, and we will see you again next week.