Welcome to KodaKoda's Weekly Immunology News, your go-to source for the latest and most exciting research coming out of the worlds of immunology and microbiology. I'm so glad you're here with me today because we have a truly packed episode. There is a lot of fascinating science to get through, so let's just dive right in.
We're going to start with a paper that caught my eye immediately because it tackles a question that researchers have been wrestling with for a long time. Why does allergic inflammation in the lungs persist for so long without burning itself out? The paper is called Progenitor T cells drive chronic pulmonary type 2 inflammation, published on August 20th 2026 in Nature Immunology. The first author is Radomir Kratchmarov from the Division of Allergy and Clinical Immunology at Brigham and Women's Hospital, Harvard Medical School in Boston.
So here's the core puzzle they were investigating. Type 2 inflammation, which is the kind of immune response that drives asthma and allergic lung disease, is coordinated by remarkably durable CD4 positive T helper 2 cells, which we call TH2 cells. But nobody really understood how these responses stay going for so long without the T cells burning out or becoming exhausted. To figure this out, the team built a mouse model of long-term pulmonary allergen exposure, basically giving mice repeated exposures to allergens over a long period of time to mimic what happens in chronic allergy. What they found was that type 2 inflammation was broadly sustained over time and there was an expanded population of cells expressing something called T cell factor 1, and these cells had a progenitor-like quality, meaning they could give rise to other cell types. In living mice, these lung TH2 progenitors were sufficient both to start and to maintain type 2 inflammation by coupling self-renewal with effector cell differentiation. In other words, these progenitor cells could make copies of themselves while also spinning off the functional cells that drive inflammation. They then used transcriptomic and spatial analysis, basically reading the gene activity of individual cells and figuring out where in the tissue those cells are sitting, to understand the full picture of chronic pulmonary TH2 responses. They found two key factors that keep the TH2 progenitors alive and well. One is interleukin-7 receptor signaling, and the other is the infiltration of B cells into the lung tissue in the context of what are called tertiary lymphoid structures, which are essentially little lymph node-like clusters that form in inflamed tissues. The data from this study define the TH2 progenitor as a distinct cellular state that arises during pathogenic chronic type 2 inflammation and plays a central role in sustaining TH2 responses over time. This is a really important finding because if we know what's keeping the fire burning, we have much better targets for treating persistent allergic lung disease.
Alright, let's move to our next paper, which takes us in a very different direction. This one is about a new drug and its effects on the trillions of microorganisms living in your gut. The title is Impact of the anti-inflammatory macrolide glasmacinal on the gut microbiota of healthy adults, an open-label trial. It was published August 20th 2026 in Nature Communications, and the first author is Tsegaye Sewunet from the Division of Clinical Microbiology at the Department of Laboratory Medicine at Karolinska Institutet in Stockholm Sweden.
So what is glasmacinal? It's an oral macrolide, which is a class of drugs that includes well-known antibiotics like azithromycin. But here's the really interesting thing. Glasmacinal has immunomodulatory properties like those antibiotics but has negligible antimicrobial activity in the lab, meaning it is not really designed to kill bacteria. It is being developed as a potential treatment to reduce exacerbations in respiratory conditions. The study was an open-label trial, where healthy participants took daily doses of glasmacinal for two weeks, and the researchers collected fecal samples to see what was happening to the gut microbiota. They used both phenotypic analysis and 16S ribosomal RNA gene sequencing, which is a standard tool for identifying and characterizing microbial communities, to evaluate the changes. What they found was that glasmacinal produced only modest effects. It reduced phylogenetic richness, which is a measure of how diverse the microbial community is in terms of evolutionary lineage, but it did not significantly affect evenness, which is how evenly distributed the different species are. It also altered beta-diversity, which is a measure of how different the microbial communities are between individuals or time points. The most affected bacterial families were Clostridiaceae, Enterobacteriaceae, and Sutterellaceae. The overall community shift was about ten percent after one week and dropped to around six percent after two weeks. When they looked at culture-based analysis, only Enterobacterales was impacted. Crucially, there was no increase in resistance to azithromycin in Enterobacterales and Bacteroides, no increase in Candida species, and no increase in Clostridioides difficile, which are all classic warning signs of antibiotic-induced gut disruption. The core anaerobic phyla of the gut, Firmicutes and Bacteroidetes, were preserved. The conclusion is that glasmacinal induced only limited restructuring of the gut microbiome, without the defining hallmarks of antibiotic-like dysbiosis. That is a meaningful distinction if this drug is ever to be used long-term in patients.
Now we have a really exciting one from the world of precision immunotherapy. This paper is titled Bispecific chimeric autoantibody receptor T cells eliminate acetylcholine receptor-specific B cells in myasthenia gravis models, published August 20th 2026 in Nature Communications. The first author is Niels von Wardenburg from the Department of Neurology with Experimental Neurology at Charité Universitätsmedizin Berlin.
Myasthenia gravis is an autoimmune neuromuscular disorder, and what happens is that the body produces autoantibodies that target the nicotinic acetylcholine receptor, or nAChR. These receptors are critically important at the neuromuscular junction, which is where nerve signals meet muscle. When the autoantibodies attack them, patients can develop severe muscle weakness and even life-threatening crises. Current therapies rely on broad immunosuppression and fail to achieve sustained remission in the majority of patients. So the researchers here developed a much more targeted approach. They engineered what they call AChR chimeric autoantibody receptor T cells, or CAAR T cells. The idea is brilliant in its logic. Rather than suppressing the whole immune system, you engineer T cells to specifically seek out and destroy the B cells that are producing the harmful anti-AChR autoantibodies. To do this, the T cells were co-transduced with CAARs that express extracellular domains of the AChR alpha-1 or beta-1 subunits. This means the engineered T cells essentially wear pieces of the acetylcholine receptor on their surface, which allows them to recognize and kill any B cell that is making antibodies against those receptor components. In testing, the AChR CAAR T cells selectively secreted effector cytokines upon activation and efficiently lysed target cells. In a xenograft mouse model, they depleted pathogenic B cell lines and reduced autoantibody levels both in the circulation and at the neuromuscular junction. These findings establish AChR CAAR T cells as a precision immunotherapy with the potential to achieve durable remission in refractory myasthenia gravis. This kind of antigen-specific targeting is really the future of autoimmune therapy.
Next up is a paper that uses the human microbiome in a completely novel way to detect cancer. The title is Mouth-to-gut microbial transmission signatures enable robust non-invasive diagnosis of gastrointestinal cancers, published August 20th 2026 in Cell Host and Microbe. The first author is Lae-Guen Jang from the Department of Systems Biology at Yonsei University in Seoul South Korea.
We know the human microbiome is spatially compartmentalized, meaning different communities of microbes live in different parts of the body. Your mouth and your gut have very different microbial populations under normal circumstances. But oral bacteria can sometimes ectopically colonize distal sites like the gut, and this may influence disease. The researchers analyzed paired oral and fecal microbiomes from 507 participants, including healthy controls and patients with metabolic disorders or gastrointestinal cancers. They developed a quantitative measure called the mouth-to-feces index, or MF index, which quantifies how much microbial transmission is happening from the mouth down to the gut. The MF index revealed elevated mouth-to-gut transmission in cancer patients, and there was a strong association with host metabolic and inflammatory indicators. Using the taxa, meaning the microbial groups, that are being transmitted between sites, the team developed a random forest classifier, which is a type of machine learning model, that accurately distinguished gastric and colorectal cancer from healthy controls across seven independent cohorts. Remarkably, the model even worked when trained solely on oral microbiome data, meaning you could potentially screen for gut cancers using just a saliva sample. When compared against the conventional fecal occult blood test, the MF-based model achieved markedly higher sensitivity. These findings uncover disease-specific transmission signatures and highlight MF microbial profiling as a non-invasive framework for gastrointestinal cancer diagnosis and risk stratification. This could genuinely change how we approach early cancer detection.
Let's keep the momentum going with a big picture perspective piece from Cell. This one is titled Neurodegeneration as a dysregulation of neuroimmune crosstalk, published August 20th 2026. The first author is F Chris Bennett from the Department of Psychiatry at the Perelman School of Medicine at the University of Pennsylvania, and also the Division of Neurology at Children's Hospital of Philadelphia.
This paper is a perspective, meaning it synthesizes a wide body of existing research rather than presenting new experimental data, but the argument it makes is profound. The central thesis is that neurodegeneration, which includes diseases like Alzheimer's and Parkinson's, should no longer be understood solely as a problem of neurons dying. Instead, it is increasingly recognized as a breakdown of the dialogue between the nervous and immune systems. Immune cells and inflammatory signals are deeply interwoven with brain function across the lifespan. Far from passive responders, immune cells act as sentinels and shapers of neuronal resilience, vulnerability, and repair. The authors argue that neurodegeneration emerges from complex interactions between neural and immune networks, positioning the immune system as both a sensor and driver of brain health. What is especially exciting is the therapeutic angle. By restoring immune homeostasis, fine-tuning inflammatory responses, or targeting epigenetic regulators of the immune state, it may be possible not only to slow degeneration but also to promote recovery. The authors outline key challenges and opportunities for this paradigm shift and highlight how a deeper integration of neuroscience and immunology could transform the future of treating neurodegenerative diseases. As someone covering immunology weekly, I find it deeply exciting that the immune system is increasingly being seen as central to conditions that we never used to think of as immune-related.
Now here is a short but very dense and interesting piece from Cell. It's titled Cuproptosis enters the cancer-immunity circuit, published August 20th 2026. The first author is Yunhao Gao from the National Cancer Center and the Chinese Academy of Medical Sciences and Peking Union Medical College in Beijing.
This is a commentary piece highlighting findings published in the same issue of Cell by Lei and colleagues. Cuproptosis is a form of cell death driven by copper accumulation inside cells, and it has been getting a lot of attention as a potential way to kill tumor cells. What Lei et al found, and what Gao's commentary explains, is a fascinating reciprocal circuit. Cuproptotic tumor cells promote dendritic cell activation and CD8 positive T cell priming, meaning when tumor cells die by cuproptosis they alert and activate the immune system. And in return, T cell-derived interferon-gamma, or IFN-gamma, sensitizes tumor cells to FDX1-dependent cuproptosis, meaning the immune response makes the tumor cells even more vulnerable to this copper-driven death. This self-reinforcing interaction provides a mechanistic rationale for combining cuproptosis induction with PD-L1 blockade to overcome immunotherapy resistance. This is the kind of positive feedback loop that researchers dream about in cancer immunotherapy.
Let me now turn to a methodological contribution that is going to matter a lot for how we evaluate vaccine research going forward. The paper is titled The VAccine cLinical study reporting gUidEline, the VALUE checklist with explanation and elaboration, published August 20th 2026 in EBioMedicine. The first author is Yuting Duan from the Evidence-based Medicine Centre at Guangzhou Medical University and the Chinese EQUATOR Centre at Hong Kong Baptist University.
The number of clinical vaccine studies published each year is large and increasing as vaccinology and biotechnology advance. Existing reporting guidelines like CONSORT for randomized clinical trials and STROBE for observational studies do not address vaccine-specific items that should be included in vaccine study reports. This matters because immunogenicity, efficacy, effectiveness, reactogenicity, and safety are all characteristics that need to be reported in a consistent and thorough way. Using the EQUATOR Network's guidance for developers of health research reporting guidelines, the team established a core working group that conducted a systematic literature review and developed an initial list of reporting elements for vaccine studies. A 42-member Delphi expert group composed of clinical vaccine researchers, methodologists, medical journal editors, and other experts then provided comments and suggestions through two rounds of Delphi surveys. The result is a final 22-item checklist across 15 domains, including 9 dedicated vaccine-specific reporting items. The checklist is called VALUE, which stands for VAccine cLinical trial reporting gUidEline, and it aims to provide a minimum set of vaccine-specific reporting items for experimental and observational clinical studies that evaluate vaccine characteristics. It complements CONSORT and STROBE by filling the gap they left. This kind of standardization work is unglamorous but genuinely important for the reliability of the scientific literature.
Next up is a brief news item from Science, but one that is scientifically and editorially significant. The piece is titled Scientists challenge unexpected finding of lymphatic vessels in bone, published August 20th 2026 in Science, written by Catherine Offord. It describes conflicting data that prompted a dispute and even a last-minute publication delay in a prominent journal. No abstract was provided but the premise is striking: a recent claim that lymphatic vessels exist inside bone has apparently generated enough scientific controversy to cause a journal to pause a planned publication. We'll keep an eye on how this one develops.
Now let's get into a really cool paper about neutrophils. The title is RAD51 stabilizes neutrophil extracellular traps to compartmentalize inflammation, published August 20th 2026 in Science. The first author is Lorenza Iolanda Tsansizi from the Antimicrobial Defence Laboratory at The Francis Crick Institute in London.
Neutrophil extracellular traps, or NETs, are web-like structures made of chromatin that neutrophils release to trap and kill pathogens. But their branched architecture has been puzzling, because nobody really knew how that branching was generated or what it was for. This study found that NET branching is mediated by RAD51, a protein that normally generates DNA junctions during DNA recombination repair. It is a remarkable example of a protein being repurposed in a totally unexpected context. Pharmacological inhibition of RAD51, as well as RAD51 knockdown, or treatment with GEN1 and RuvC resolvases, which are enzymes that cut DNA junctions, all reduced branching and destabilized NETs. Conversely, RAD51 upregulation generated NETs with variable stability. To test what this means during infection, the researchers inhibited RAD51 during murine pulmonary Aspergillus fumigatus infection, a fungal infection that can be dangerous especially in immunocompromised patients. Dismantling NETs this way reduced lung cytokines, which sounds potentially beneficial, but there was a catch. The increased accumulation of NET components in the circulation led to interleukin-6 induction in circulating monocytes, which exacerbated type 2 inflammation and asthma. In human aspergillosis patients, extracellular plasma DNA correlated with IL-6 and eotaxin. The conclusion is that by structurally stabilizing NETs, RAD51 compartmentalizes inflammation locally in order to prevent aberrant systemic immune activation. This elegantly links DNA repair biology to innate immune function and inflammatory disease.
Here is a beautiful piece of fundamental neuroscience-meets-immunology work. The paper is titled Functional role of skull lymphoid structures in CNS immunosurveillance, published August 19th 2026 in Nature. The first author is Jang Hyun Park from the Brain Immunology and Glia Center at Washington University in St Louis.
We have known for a while now that the central nervous system is not completely isolated from the peripheral immune system, but the mechanisms of CNS immunosurveillance have remained incompletely understood. Recent findings showed that channels between the skull and the dura mater facilitate the exchange of cerebrospinal fluid and immune cells between the CNS and skull bone marrow in mice. Skull bone marrow was already known to be a source of immune cells for the CNS, but its role in antigen-specific adaptive immune responses was unclear. This study identifies lymphoid structures within the skull bone marrow that feature germinal center-like formations and contain a distinct population of follicular-helper-like T cells that promote B cell activation and humoral immunity through CD40L, IL-21, and IFN-gamma signaling. These adaptive immune cells within the skull bone marrow lymphoid structures surveil and respond to CNS-derived antigens and contribute to anti-tumor immune responses in mouse brain cancer models. So your skull is not just a protective shell. It contains specialized immune structures that are actively monitoring and responding to what is happening in your brain. This is a paradigm-shifting finding for neuroimmunology.
Moving along, we have a paper on highly pathogenic avian influenza and its effects on wild bird populations. The title is Avian influenza amplified age-related mortality in a long-lived seabird, published August 19th 2026 in Nature Communications. The first author is Wouter Courtens from the Research Institute for Nature and Forest in Brussels, Belgium.
Using 28 years of ringing data along with individual-level data from the 2022 mass mortality event in northwestern European Sandwich terns, the researchers found something that had not been clearly documented before. Mortality from highly pathogenic avian influenza A H5N1 clade 2.3.4.4b was biased towards older individuals, while no sex bias was observed. HPAI-related mortality increased from approximately 5 to 10 percent in young breeders to more than 40 percent in the oldest individuals. This age-biased loss likely removed the most experienced individuals from the population, which could have serious consequences for population resilience since experience matters enormously in long-lived species. The findings highlight a previously underappreciated mechanism through which HPAI outbreaks may impair the long-term survival of long-lived avian populations, and given that H5N1 continues to spread globally, this has real conservation implications.
Now here is one that connects to a topic that has been generating a lot of public interest lately: supercentenarians and the secrets of extreme longevity. The paper is titled CD4 CTLs in supercentenarians, signs of adaptive expansion in healthy aging, published August 19th 2026 in Cell Reports. The first author is Kosuke Hashimoto from the Institute for Protein Research at The University of Osaka and RIKEN Center for Integrative Medical Sciences in Yokohama.
A previous study had identified CD4 cytotoxic T lymphocytes, or CD4 CTLs, as a hallmark of supercentenarians, meaning people aged 110 and above. CD4 CTLs have primarily been studied in disease contexts, but their role in healthy aging was unclear. Using single-cell immune profiling of T cells from supercentenarians, the researchers found that CD4 CTLs begin to expand around the age of 100, characterized by sequential CD27 and CD28 loss without exhaustion. That is important: they are differentiating and becoming more specialized, but they are not burning out. These CD4 CTLs were dominated by large clones, with top clones averaging 33.3 percent, indicating repeated stimulation by persistent antigens. Furthermore, CDR3 beta sequences of the top clones matched those of T cells expanded in tumors, particularly lung cancer, suggesting these cells may be targeting cancerous cells. Ex vivo stimulation experiments revealed that CD4 CTLs consist of subgroups defined by interleukin expression patterns, suggesting their plasticity within the same clone. The findings suggest that CD4 CTLs expand and diversify as an adaptation to persistent antigens, potentially contributing to longevity through cancer suppression. So one of the secrets to living past 110 might be a specialized population of T cells that quietly keeps cancer in check over decades.
Let's talk about gut bacteria and heart health. The paper is titled Gut microbiota generate dinitrosyl iron complexes with cardiometabolic benefits, published August 19th 2026 in Cell. The first author is Andrei L Kleschyov from the Department of Physiology and Pharmacology at Karolinska Institutet in Stockholm.
We know gut bacteria affect host physiology in all kinds of ways, but the mechanisms are not always understood. This study identifies a really novel pathway. Gut microbes can convert inorganic nitrate and non-heme iron into mobile bioactive dinitrosyl iron complexes, abbreviated as DNICs, which are then distributed systemically and affect host metabolism. The researchers used electron paramagnetic resonance to detect DNICs in tissues of conventional but not germ-free mice, confirming that the gut microbiome is essential for their production. Mouse and human feces as well as E. coli generated DNICs from nitrate and iron citrate, while a nitrate-reductase-deficient mutant did not, pinpointing the mechanism. Dietary supplementation with nitrate plus iron citrate or with synthetic DNICs increased tissue DNIC levels and ameliorated cardiometabolic dysfunction in mice fed a Western diet. In HepG2 cells and human hepatocyte spheroids, DNICs reduced fatty acid-induced steatosis, which is fat accumulation in the liver. Interestingly, DNIC bioactivity is mediated by the iron-nitric oxide entity rather than by free nitric oxide itself, and the mechanism involves activation of soluble guanylyl cyclase, inhibition of leucine uptake, and normalization of mTORC1 signaling. Modulating DNIC formation by the gut microbiota could be a strategy to support cardiometabolic health, and this finding opens up a genuinely new way of thinking about how diet, microbes, and metabolism interact.
Next we have a very innovative paper from the field of cancer immunotherapy. The title is Synthetic transcription factors designed by domain recombination enhance CAR T cell antitumor function, published August 19th 2026 in Cell. The first author is Oliver Takacsi-Nagy from the Department of Pathology and the Center for Immunotherapy Design at Stanford University.
Human protein-coding genes evolved via rearrangement of domains from ancestral genes, and this team took inspiration from that evolutionary process to develop a scalable method to assemble novel genes from constituent domains within a protein family. They call this DESynR, which stands for domain engineered via synthesis and recombination. In primary human T cells, DESynR activator protein-1, or AP-1, transcription factors significantly outperformed natural AP-1 transcription factors across both in vitro and in vivo antitumor assays. These DESynR AP-1 transcription factors induced broad transcriptional and epigenetic reprogramming and established non-natural T cell states that optimized features of exhaustion resistance, effector function, cytotoxic function, and persistence, sometimes co-opting gene modules from completely different cell types. The reprogramming was primarily driven by differential regulation of established AP-1-bound regulatory elements rather than unique binding sites. The researchers also screened DESynR erythroblast transformation-specific and forkhead box transcription factors to show generalizability across protein families. Overall, this work demonstrates that reconfiguring existing protein domains may uncover non-evolved genes that program therapeutically relevant cell states, which is a powerful new tool for engineering better CAR T cells.
Now let's talk about a paper with important implications for antiviral vaccines. The title is RNA structures regulate norovirus life cycle and enable rational attenuation in vivo, published August 19th 2026 in Cell. The first author is Tanja Hann from the Department of Molecular Biophysics and Biochemistry at Yale University.
Norovirus is one of the most common causes of acute gastroenteritis worldwide, and despite this there is no approved vaccine. Viral genomes encode regulatory RNA structures that orchestrate key steps of viral replication and gene expression. This team systematically mapped and functionally interrogated structured RNA elements across the murine norovirus genome using orthogonal in-cell chemical probing, revealing conserved motifs that regulate viral function. When they disrupted specific structural elements, viral replication was reduced in cell culture, translation was modulated in what they describe as cis, meaning locally along the same RNA molecule, and viral RNA levels decreased in animal infection models. Building on these findings, the team rationally designed a genetically stable, attenuated virus, meaning a weakened version that can still be recognized by the immune system. This attenuated virus elicited protective immunity and limited viral replication upon secondary challenge. The work uncovers essential roles for RNA structure in norovirus biology and establishes a generalizable framework for RNA structure-guided design of antiviral vaccines and therapeutics. This is a landmark contribution for RNA virology.
Let me now cover three more papers with abstracts before we wrap up with our no-abstract section. First, Mitochondrial profiling across macrophage states reveals inhibition of IL-4/IL-13 reprogramming by the integrated stress response, published August 21st 2026 in Science Advances. The first author is Joan Blanco-Fernandez from the Department of Immunobiology at the University of Lausanne.
This paper investigates the role of mitochondria in macrophage reprogramming. Macrophages can shift their function dramatically depending on what signals they receive from the environment, and this study integrates transcriptomics with whole-cell and purified mitochondrial proteomics to profile macrophages stimulated by either LPS and interferon-gamma, which drives inflammatory activation, or by interleukin-4 and IL-13, which drives an alternative anti-inflammatory state. The researchers reveal a notable disconnect between mitochondrial transcript and protein levels following either stimulus. In IL-4 and IL-13 macrophages, there is a STAT6-dependent increase in mitochondrial DNA expression and intramitochondrial translation. Inhibition of ATP synthase uniquely triggers a heme-regulated inhibitor-dependent integrated stress response through mitochondrial hyperpolarization, which prevents IL-4 and IL-13 reprogramming. Restoring mitochondrial membrane potential or inhibiting the integrated stress response rescues IL-4 and IL-13 mediated reprogramming. The key takeaway is that mitochondrial DNA expression, intramitochondrial translation, and mitochondrial membrane potential are critical, drug-sensitive determinants of how macrophages respond to IL-4 and IL-13 signals.
Second from Science Advances, published August 21st 2026, is Central T cell tolerance from sparse peptide sampling, with first author Hannah V Meyer from the Simons Center for Quantitative Biology at Cold Spring Harbor Laboratory.
This paper addresses a beautifully fundamental question about how the immune system avoids attacking the body's own tissues. Negative selection in the thymus limits autoimmunity by eliminating T cells that react strongly to self-antigens. But individual T cells are only exposed to a small fraction of all self-peptides during their training in the thymus. How does tolerance then generalize to the remaining self-peptides found in peripheral tissues throughout the body? The researchers show that this generalization can be achieved because the immune system satisfies two conditions necessary for generalization in machine learning settings. Consequently, sparse, random sampling of only 10 percent of self-peptides in the thymus is sufficient to avoid reactivity to 90 percent of peripheral self-peptides. They support this result and validate predictions from their model with diverse experimental data. This provides a plausible quantitative answer to a long-standing question underlying adaptive immunity, and it elegantly connects immunology to the mathematics of learning algorithms.
Our last paper with a full abstract is partially listed, titled Unconventional role of hydroxymethylglutaryl-CoA synthase 1 in driving pathogenic TH17 cell immunity and autoimmune diseases, from Science Advances published August 21st 2026. The first author is Jie Sun from the Department of Urology and State Key Laboratory of Virology and Biosafety at a research institute in China, though the full institutional information was truncated in our source. The title alone signals something important: this is about an enzyme in the cholesterol synthesis pathway, specifically hydroxymethylglutaryl-CoA synthase 1, playing an unexpected role in driving the TH17 cells that are central to many autoimmune conditions. We will bring you the full details on this one as more information becomes available.
And now, before we close out, let's quickly run through the papers we know about that do not have abstracts yet but are absolutely worth your attention.
From Nature Medicine, there's a paper by Karen O'Leary on intercepting pancreatic cancer with a vaccine, and another piece examining how county-level surveillance failed to detect that measles transmission had reached epidemic thresholds in schools, which has serious public health implications.
From Nature, Rachel Fieldhouse has a piece on Moderna's cancer vaccine stopping melanoma from returning and what that means for personalized treatments. And there is another Nature piece by Katherine Bourzac asking how people live beyond 110, with the answer pointing to an abundance of cancer-killing cells, which ties in nicely with the supercentenarian paper we discussed earlier. There is also an untitled Nature piece about how a virus deploys what they describe as a loose cannon enzyme to overpower bacterial defences, which sounds like it could be a fascinating piece of phage biology.
From Nature Immunology, there are several pieces worth noting. There is a paper by Holm Uhlig from the Centre for Human Genetics at the University of Oxford on regulatory CD8 positive T lymphocytes controlling intestinal inflammation, which is a significant topic in mucosal immunology. There is also a piece on antigen-sampling gut cells moonlighting as organizers of immune defense, and a paper by Ruth Montgomery from Yale School of Medicine titled From data to discovery, a unified framework for human immunology, which sounds like an important integrative resource for the field. There are also two commentary pieces in Nature Immunology, one by Purbita Bandopadhyay from the University of Minnesota on AXL positive DC3s and Notch signaling, and one by Susan Westfall from McGill University on NOD2 signaling in the endothelium for gut immunity. And there is an author correction from Xinhui Ni at East China Normal University on IL-17D-induced inhibition of DDX5 expression in keratinocytes.
From Gastroenterology, there is a paper by Jostein Ibsen from the Norwegian Coeliac Disease Research Centre on targeted serum proteomics revealing profiles associated with gut pathology in celiac disease, and another study on specific epigenetic alterations that precede the diagnosis of inflammatory bowel disease in adults in Northern Europe.
And finally from Nature Medicine, there is a piece on the px1 locus being linked to declining susceptibility to malaria drugs in Uganda, which is a very important finding for global infectious disease.
That is a wrap on this week's episode of KodaKoda's Weekly Immunology News. What an incredible week it has been for the field. From progenitor T cells sustaining chronic allergic inflammation, to skull bone marrow acting as a sentinel for the brain, to gut microbes making molecules that protect the heart, the breadth and depth of immunology and microbiology research never ceases to amaze me. Thank you so much for listening, and I will see you next week with more of the latest from the frontlines of science.