🧬 KodaKoda's Weekly Immunology News

Welcome to KodaKoda's Weekly Immunology News. I am so glad you are here with me today. We have got a really packed episode this week covering everything from tumor microenvironments and immune evasion to some fascinating new findings about inflammasome biology and even a story about HIV capsids doing something completely unexpected in the nucleus. Let us dive right in. We are starting with a paper out of Science Advances published on August 7th 2026. The title is The microenvironment dictates glyco-immune surveillance via HSF1-mediated metabolism and the first author is Kevin M Tharp from the Cancer Metabolism and Microenvironment Program at the NCI-Designated Cancer Center at Sanford Burnham Prebys Medical Discovery Institute in La Jolla California. So here is a really interesting question this paper is wrestling with. We know that solid tumors have this altered glucose metabolism going on but is that something that is baked into the tumor cells themselves or is it actually a response to the environment around them. Think of it like asking whether someone is stressed because of who they are or because of where they are. The researchers used normal epithelial cells and cultured them in a physiological medium under conditions designed to mimic either healthy or cancerous tissue. Then they built out what they call multiomics relationships basically connecting the dots between the biochemical and physical properties of the environment and what that environment does to the cell's biosynthetic outputs when glucose metabolism is altered. And here is what they found. Microenvironmental properties like hyperglycemia which just means too much glucose in the surroundings can actually change the composition and thickness of something called the glycocalyx. The glycocalyx is basically this sugar coating on the surface of cells and it turns out its thickness matters a lot for immune surveillance. The thicker or differently composed it is the harder it can be for immune cells to recognize and attack tumor cells. This effect was linked in part to a mechanosensitive stress response pathway involving a protein called Heat Shock Factor 1 or HSF1. The team then looked at this HSF1 and hyperglycemia axis in actual human breast tumors and they validated it as a druggable vulnerability meaning you could potentially target it to license natural killer cell lethality against cancer cells. Natural killer cells are part of our innate immune system and they are supposed to recognize and destroy abnormal cells like tumor cells so unlocking that ability is a really exciting prospect. Next up also from Science Advances on August 7th 2026 we have Formation of tertiary lymphoid structures drives Parkin antitumor immunity from first author Michela Perego at the Genome Regulation and Cell Signaling Program at The Wistar Institute in Philadelphia Pennsylvania. This one is about mitochondria and cancer which is a combination you might not immediately put together. We know mitochondria can activate immunity but their specific role in cancer has not been well understood. This team looked at Parkin which is a regulator of mitochondrial fitness and they found that transgenic expression of Parkin meaning they got cells to overexpress this protein induces inflammation and interferon gene signatures and suppresses prostate cancer formation. That alone is interesting but what really caught my attention is what happened to the immune landscape inside the prostate. They found CD8 positive and CD20 positive immune aggregates forming within the tumor tissue and these had hallmarks of what are called mature tertiary lymphoid structures or TLS. Now TLS are like pop-up lymph nodes that form inside tumors. They are associated with better prognosis in many cancers and they represent organized immune activity happening right at the site of disease. These structures in the Parkin-expressing tumors showed markers of B cell maturation like CXCL13 and CCL21 germinal center formation through BCL6 and GL7 mature dendritic cells and high endothelial venules marked by LYVE-1. The Parkin TLS also showed high immunoglobulin gene expression and recruited CXCR5 positive follicular T helper cells along with expanded CD69 positive and KLRG1 positive effector T cells. The conditioned medium from Parkin-positive cells expanded memory B cells and plasma cells increased IgG1 production and sustained B and T cell migration. And when they conditionally expressed Parkin in vivo TLS formed immunoglobulin chains were upregulated and prostate cancer growth was inhibited. But here is the key mechanistic finding. When Parkin was reconstituted in mice that lacked IFNAR1 or CD8 or CD20 there was no effect. So the antitumor benefit depends on all of those components being present. The conclusion is that mitochondrial immunity orchestrates antitumor responses and TLS formation is a major driver of tumor suppression. Still in Science Advances from August 7th we have a study with implications for aging and immune function. The title is Ly6d expression delineates two putative postnatal thymus epithelial progenitor cells that are differentially affected by aging and the first author is Irene Calvo-Asensio from the Department of Biomedicine at the University of Basel and University Children's Hospital in Basel Switzerland. The thymus is where T cells are educated and mature. It is absolutely central to adaptive immunity. But the thymus shrinks as we age and we lose thymic function over time which is one reason older people have weaker immune responses. A big open question has been about thymic epithelial progenitor cells or TEPCs. These are the cells that maintain the thymic epithelium. We have not known exactly which cells they are after birth or whether there are bipotent progenitors that can give rise to both major types of thymic epithelial cells or whether separate lineage-restricted progenitors maintain separate compartments independently. This study used an inducible lineage-tracing system based on expression of the thymoproteasomal protein beta5t which is expressed in embryonic and a subset of postnatal TEPCs to track how progenitors and their descendants relate to each other over time. They identified two potential lineage-biased progenitor subpopulations distinguished by expression of a marker called Ly6d. What is particularly striking is that aging disproportionately affects the Ly6d negative subpopulation compared to Ly6d positive TEPCs. That difference has real implications for strategies aimed at rejuvenating aging thymic epithelia. This study contributes to our understanding of TEC lineage developmental pathways and could inform future approaches to enhancing thymic function in the context of aging and disease. Now we are going to take a brief detour into microbiology because this next paper from Science Advances is directly relevant to antibiotic resistance which is a massive global health problem. Published August 7th 2026 the title is Structural insights into a substrate translocation pathway revealed by the RND efflux pump complex MexJK from Pseudomonas aeruginosa and the first author is Zhikun Wu from the Ministry of Education Key Laboratory of Combinatorial Biosynthesis and Drug Discovery at the School of Pharmaceutical Sciences at Wuhan University in China. Pseudomonas aeruginosa is a particularly dangerous opportunistic pathogen that causes life-threatening infections especially in immunocompromised patients. One of the major reasons it is so hard to treat is a family of molecular machines called RND efflux pumps. RND stands for resistance-nodulation-cell division. These pumps actively push antibiotics out of the bacterial cell before they can do their job. MexK is a narrow-spectrum RND transporter and it works together with a membrane fusion protein called MexJ and outer membrane proteins to form a tripartite efflux complex that efficiently exports drugs including triclosan. What the researchers did here was resolve the cryo-electron microscopy structures of apo-MexK at 3.4 angstrom resolution and the triclosan-bound MexJK complex at 2.6 angstrom resolution. What they found was a triclosan-binding pocket within the transmembrane domain of MexK that is distinct from known substrate-binding sites in other RND transporters. Using molecular dynamics simulations and mutagenesis they characterized a previously unrecognized triclosan transport tunnel that crosses the inner membrane and has cytosolic access. They also showed that the key residues for triclosan efflux are essential for two other potential substrates of MexK which are chloramphenicol and pyrimethamine. This gives us the molecular basis for an unusual drug trafficking pathway in RND efflux pumps and that kind of structural knowledge is exactly what drug developers need to design inhibitors that could block these pumps. Back to tumor immunology now. Also from Science Advances on August 7th 2026. The title is APOE positive macrophages and POSTN positive CAFs form immune-exclusion niche driving immunotherapy resistance in clear-cell renal carcinoma and the first author is Qintao Ge from the Department of Urology at Fudan University Shanghai Cancer Center in Shanghai China. Immune checkpoint blockade therapies have been a revolution in cancer treatment but a lot of patients do not respond to them and we often do not know why. This paper digs into the biology of treatment resistance in clear cell renal cell carcinoma which is the most common type of kidney cancer. The researchers focused on tumor immune barriers which they call TIBs. These are spatially organized niches made up of stromal and immune components that physically restrict lymphocytes from entering the tumor. They mapped TIBs in clear cell renal cell carcinoma and identified a peritumoral variant built from POSTN positive cancer-associated fibroblasts interlaced with APOE positive tumor-associated macrophages. This combination excluded CD8 positive T cells from tumor cores and was enriched in patients with poor prognosis who did not respond to immune checkpoint blockade. Using spatial transcriptomics and single-cell profiling they showed these TIB regions are enriched for extracellular matrix remodeling immunosuppressive ligand-receptor circuits and metabolic reprogramming. Mechanistically tumor-derived TGF-beta1 activated cancer-associated fibroblasts through SMAD signaling inducing POSTN expression and recruiting APOE positive tumor-associated macrophages through integrin and chemokine axes. The macrophages then secreted TGF-beta1 and VEGFA which amplified stromal programs and sustained exclusion creating a vicious cycle. When they blocked POSTN it reprogrammed macrophages reduced matrix-mediated suppression and restored CD8 T cell infiltration. In vivo POSTN inhibition combined with immune checkpoint blockade boosted antitumor immunity reduced tumor burden and reversed immunosuppressive infiltration. This is a really strong case for POSTN as a therapeutic target. Now for something genuinely clever from Science Advances August 7th 2026. The title is T cell-nanodrug conjugates synchronize vascular normalization and immune activation for solid tumor therapy and the first author is Xin Yang from the School of Pharmaceutical Sciences at Shenzhen Campus of Sun Yat-sen University in Shenzhen China. Adoptive T cell therapy is one of the most exciting frontiers in cancer treatment where you take immune cells from a patient engineer them and put them back to fight cancer. But there is a big practical problem. Solid tumors build up abnormal vasculature that physically prevents T cells from getting in. On top of that the tumor microenvironment suppresses T cell function even when they do get there. This team used a drug called lenvatinib to induce what they call transient vascular normalization meaning they temporarily fix the leaky and poorly organized blood vessels in tumors to make it easier for T cells to infiltrate. They also found that lenvatinib enhances T cell persistence by promoting differentiation toward a memory phenotype and this works by suppressing the PI3K-AKT-mTOR pathway which normally drives effector differentiation and by activating FOXO1 a transcription factor that promotes memory formation. But here is the real engineering innovation. To coordinate the timing of vascular normalization with T cell enhancement they linked lenvatinib-loaded PD-L1-blocking micelles to T cells through acid-labile click chemistry. This creates pH-responsive T cell-nanodrug conjugates that release their payload specifically in the acidic tumor environment. The conjugates synchronize intratumoral release of lenvatinib and a PD-L1 antagonist peptide called OPBP-1 thereby coordinating vascular normalization T cell differentiation and checkpoint blockade all at once. In vivo in B16-OVA tumors the conjugates increased intratumoral CD8 positive T cells and splenic memory T cells by over sixfold and achieved complete tumor regression in a subset of MC38-OVA tumors without systemic toxicity. Okay now over to virology with a paper also from Science Advances published August 7th 2026. The title is Capsid stabilization reprograms the nuclear fate of the HIV genome and the first author is Thierry Mourer from the Virology Department at Institut Pasteur in Paris France. This study looks at Lenacapavir which is a first-in-class capsid inhibitor for HIV. The capsid is the protein shell that surrounds the viral genetic material. The idea behind Lenacapavir is to stabilize this capsid so it cannot open properly and the virus cannot replicate. Previous understanding was that this drug worked by disrupting reverse transcription or nuclear import of the viral genome. But this study found something different. At low nanomolar concentrations Lenacapavir impeded HIV-1 replication in macrophages without disrupting reverse transcription or nuclear import. Using ultrastructural analyses in Lenacapavir-treated cells they found preserved conical capsids persisting within nuclear CPSF6-enriched puncta which are HIV-1-induced membraneless organelles. These organelles remained spatially segregated from canonical integration hubs near nuclear speckles. Instead of fusing with nuclear speckles these HIV-1 membraneless organelles were rerouted to chromatin-associated promyelocytic leukemia nuclear bodies known as PML-NBs and molecular exchange occurred without condensate fusion. This nuclear redirection correlated with sequestration of the viral genome inside the stabilized capsids reducing the pool of viral DNA available for integration and redirecting the few accessible genomes to atypical integration sites near PML-NBs which are more repressive environments for gene expression. So Lenacapavir is essentially sending the HIV genome to the wrong neighborhood in the nucleus where it cannot do as much damage. That is a really elegant mechanism. Now let us talk vaccines. Still Science Advances August 7th 2026. The title is ZPY-CpG-Ch a broad coverage vaccine against Streptococcus pneumoniae and the first author is Teerawit Audshasai from the Department of Clinical Infection Microbiology and Immunology at the Institute of Infection Veterinary and Ecological Sciences at the University of Liverpool in the UK. So we have existing pneumococcal vaccines like Prevnar-13 and its higher-valency successors and they have done a lot of good in reducing invasive pneumococcal disease globally. But their effectiveness is increasingly threatened by multidrug-resistant strains and serotype replacement which is when the circulating serotypes shift toward ones not covered by the current vaccines. This is a real and growing problem. This study reports the preclinical development of ZPY-CpG-Ch a broad-coverage protein-based pneumococcal vaccine formulation. They tested it in translational murine models using both adult and neonatal mice and assessed various adjuvants protein combinations and doses followed by challenge experiments with both vaccine-covered and non-vaccine-covered serotypes. Prevnar-13 was included as a benchmark and it showed robust efficacy but ZPY-CpG-Ch achieved greater cross-serotype protection. The researchers attribute this enhanced efficacy primarily to TH17-biased immune responses meaning the vaccine skews immunity toward a type of T helper response that is particularly effective at mucosal surfaces where Streptococcus pneumoniae tends to cause disease. This is an important step toward a truly universal pneumococcal vaccine. Next from Science Advances August 7th 2026 we have a study combining epigenetics tumor biology and immunotherapy in melanoma. The title is Transposable elements and homotypic niches drive immune dynamics and resistance in melanoma epigenetic-based immunotherapy and the first author is Erika Ciervo from the Sylvester Comprehensive Cancer Center at the Miller School of Medicine at the University of Miami. Melanoma is well known for its ability to switch between different cell states which helps it evade immunity and resist treatment. This paper profiled longitudinal biopsies from patients with melanoma treated in the phase 1b NIBIT-M4 epi-immunotherapy trial which combined a DNA methyltransferase 1 inhibitor with an anti-CTLA-4 antibody. They used single-cell multiome and spatial transcriptomics to get a detailed picture of what was happening. They identified seven malignant meta-programs including a rare Wnt/beta-Catenin melanocytic state and a dedifferentiated neural crest-like state that was enriched in patients who did not respond to therapy. Spatial analyses showed that homotypic clustering meaning tumor cells of similar types grouping together stabilizes these resistant programs with neural crest-like cells forming compact niches. Responders showed enrichment of an antigen presentation and interferon program along with coordinated T and B cell expansion whereas nonresponders retained stable neural crest-like clusters. The epigenetic therapy reactivated transposable elements which primed innate immunity and enhanced immunogenicity. A transcription factor called NFATC2 emerged as a master regulator of the neural crest-like states and resistance and when it was perturbed it promoted differentiation and immunogenicity. The paper nominates beta-Catenin and NFATC2 as therapeutic vulnerabilities in melanoma. Now we are moving into what I think is the most exciting cluster of papers this week because we have not one not two but three research articles published in Science Immunology on August 7th 2026 all converging on the same molecule and the same inflammasome pathway. Plus there are two companion pieces commenting on them. This is one of those rare moments in science where multiple independent groups discover something simultaneously and it fundamentally changes how we understand a disease. The inflammasome is an intracellular protein complex that senses danger signals and triggers a form of inflammatory cell death called pyroptosis as well as the release of pro-inflammatory cytokines. The pyrin inflammasome in particular is mutated in a hereditary disease called familial Mediterranean fever and related autoinflammatory diseases. The key question that has been lingering is exactly how pyrin gets activated at a molecular level. The first of the three research articles is A genotype-first approach reveals the molecular basis of pyrin inflammasome activation published in Science Immunology August 7th 2026 by first author Naoya Iwata from the Department of Pediatrics at Kyoto University Graduate School of Medicine in Kyoto Japan. Mutations in the MEFV gene which encodes the pyrin protein are associated with a spectrum of inflammatory conditions called pyrin-associated autoinflammatory diseases or PAADs. There are 400 MEFV variants listed in the Infevers database and most of them are classified as variants of uncertain significance which makes genetic diagnosis incredibly difficult. This team used a cell-based pyroptosis assay to stratify 265 missense MEFV variants and identified previously uncharacterized pathogenic variants. They then characterized the interaction between the pyrin B30.2 domain and a protein called CDC42 which is a key regulator of pyrin intracellular trafficking and activation. They found that classical familial Mediterranean fever related variants bind tightly to CDC42 to induce pyrin hyperactivation. But certain non-familial Mediterranean fever variants induce pyrin hyperactivation independently of CDC42 suggesting there are multiple pathways involved in pyrin activation. This genotype-first approach could really advance how we understand and diagnose complex autoinflammatory diseases. The second research article in this trio is An N-terminal CDC42 T43I variant reveals the mechanism of pyrin inflammasome activation also in Science Immunology August 7th 2026 by first author Mariko Aoki also from the Department of Pediatrics at Kyoto University Graduate School of Medicine in Kyoto Japan. Here the team identified a heterozygous amino-terminal variant in CDC42 specifically a change where threonine at position 43 is replaced by isoleucine called p.T43I. This was found in patients with autoinflammation. They uncovered a molecular link between CDC42 and the inflammasome sensor pyrin. They demonstrated that the region surrounding residue T43 of CDC42 interacts with the carboxyl-terminal B30.2 domain of pyrin and regulates its localization and activation. The T43I substitution strengthens the CDC42-pyrin interaction through additional van der Waals interactions leading to increased pyrin inflammasome activation as evidenced by increased ASC speck formation enhanced pyroptosis and excessive interleukin-1 beta and IL-18 production. This identifies CDC42 as a pyrin ligand and suggests that pyrin is dually regulated by two RHO family GTPases namely RHOA and CDC42. The third research article is An autoinflammatory CDC42 variant M45L demonstrates the mechanism of pyrin inflammasome activation in Science Immunology August 7th 2026 by first author Shouya Feng from the Centre for Innate Immunity and Infectious Diseases at Hudson Institute of Medical Research in Clayton Victoria Australia. This group independently discovered a different CDC42 variant at a nearby position. CDC42 methionine-45 to leucine which they call M45L. They confirmed its pathogenicity by showing it promotes pyrin inflammasome activation consistent with highly elevated circulating interleukin-18 in all affected individuals. Using coimmunoprecipitation they showed that CDC42 interacts with both the PYD and B30.2 domains of pyrin and the B30.2 interaction is greatly enhanced by the M45L variant. Structural models show that CDC42 methionine-45 sits in a hydrophobic cleft of the pyrin B30.2 domain. They propose a model where CDC42 nucleates pyrin via the B30.2 domain and after a threshold is reached the PYD domain is liberated to drive inflammasome activation. Importantly blocking the inflammasome-associated cytokine IL-1 was therapeutically effective in patients with this condition. And accompanying all three of these research articles is an editorial perspective titled Misfirin apostrophe pyrin published in Science Immunology August 7th 2026 by Fiachra Humphries from the Division of Innate Immunity in the Department of Medicine at UMass Chan Medical School in Worcester Massachusetts. The piece identifies CDC42 as a binding partner of the pyrin B30.2 domain and frames this as a previously unrecognized mechanism regulating pyrin inflammasome activation tying together all three studies in a coherent narrative. There is also a fourth piece in Science Immunology this week that is worth mentioning briefly. It is a perspective titled Mist-ical memory the airway defenses induced by FluMist vaccination in adults by first author Huzaifa Zohair from the Department of Microbiology and Immunology at the Renaissance School of Medicine at Stony Brook University in New York. This piece highlights a study using longitudinal nasopharyngeal swabs to sample and reveal upper airway humoral memory generated after intranasal FluMist vaccination. The emphasis on mucosal immunity and intranasal vaccination is really timely given how much interest there is in next-generation respiratory virus vaccines. Also there is a perspective in Science Immunology from August 7th titled PKM2 works off the books to drive effector T cell function in MS by Alexia Falle from the Department of Molecular Medicine at the Faculty of Medicine at Universite Laval in Quebec City Canada. This piece explores the noncanonical functions of PKM2 an enzyme usually associated with glycolysis and shows that these alternate functions drive pathogenic T cell activity in patients with multiple sclerosis. It is a nice reminder that metabolic enzymes often do a lot more than just their textbook job. Now we have a really important paper from PNAS published August 11th 2026. The title is T cell-intrinsic AIM2 exacerbates lung inflammation in OVA-LPS- and HDM-induced asthma models and the first author is Wei-Chun Chou from the Lineberger Comprehensive Cancer Center at the University of North Carolina Chapel Hill. Asthma is a heterogeneous inflammatory airway disease characterized by immune dysregulation airway hyperresponsiveness and excessive immune activation. NLRP3 which is a well-known inflammasome sensor has been studied a lot in asthma but its role has been controversial. The DNA sensor AIM2 which stands for Absent in Melanoma 2 had not been well characterized in asthma. This team analyzed public human datasets and found increased AIM2 but not NLRP3 expression in severe asthma and in neutrophilic compared with paucigranulocytic asthma. In allergic asthma models induced by ovalbumin and lipopolysaccharide or house dust mite AIM2 expression was increased in lung homogenates and bronchoalveolar lavage fluid cells. Single-cell RNA-sequencing data showed increased Aim2 but not Nlrp3 expression in T helper cells with most Aim2-expressing cells coexpressing Gata3 which is a key transcription factor for type 2 immunity. In the OVA-LPS model whole-body Aim2 deficiency reduced airway hyperresponsiveness inflammatory cytokine production airway smooth muscle actin and a marker of DNA damage called gamma-H2A.X consistent with decreased airway remodeling and tissue stress. And here is the unexpected finding that makes this paper really stand out. CD4-specific deletion of Aim2 but not Treg-specific or myeloid-specific deletion significantly attenuated disease. So the AIM2 that matters most in asthma is the AIM2 that is inside CD4 positive T cells. Myeloid AIM2 also had a role but it modulated different aspects of disease including IgG1 and IL-13-producing CD4 T cells and alveolar macrophages. This work establishes AIM2 as a regulator of allergic asthma acting predominantly through T cells. From Cell Reports published August 7th 2026 we have a paper about bile acids metabolism and liver disease. The title is Hyodeoxycholic acid suppresses hepatic steatosis in a PPARalpha-dependent manner via distinct GLP-1- and iNKT cell-mediated pathways and the first author is Eunyoung Lee from the Department of Medical Physiology at Chiba University Graduate School of Medicine in Chiba Japan. Hepatosteatosis which is the accumulation of fat in the liver is a really common metabolic disorder and it sits at the root of a lot of serious liver disease. Bile acids are known to influence hepatosteatosis immune function and incretin secretion but the specific mechanisms have not been clear. This study identified that supplementation with hyodeoxycholic acid which they abbreviate as HDCA in high-fat diet-fed mice increases hepatic iNKT cells and elevates circulating GLP-1 and both of those effects upregulate fatty acid oxidation genes in a PPARalpha-dependent manner. Mechanistically HDCA increases iNKT cells and IFN-gamma production which promotes hepatic lipid catabolism and thereby attenuates triglyceride accumulation in wild-type mice but not in iNKT cell-deficient mice or PPARalpha knockout mice. In contrast the GLP-1 receptor agonist suppresses high-fat diet-induced steatosis in wild-type and iNKT cell-deficient mice but not in PPARalpha knockout mice or GLP-1 receptor knockout mice. Furthermore the anti-steatotic effect of HDCA is nullified in GLP-1 receptor knockout mice. So putting it all together HDCA alleviates hepatosteatosis through two distinct but converging mechanisms. One is an iNKT cell and IFN-gamma immunometabolic pathway and the other is a GLP-1-dependent pathway. The finding that a single bile acid can engage both immune and endocrine pathways to protect the liver from fat accumulation makes HDCA a really interesting candidate for multi-target therapeutic strategies. And finally before we wrap up with some brief mentions the last abstract paper this week comes from the Journal of Experimental Medicine published September 7th 2026. The title is Overcoming immunogenic gaps in malaria subunit vaccines by broadening CSP regions targeted and the first author is Ja-Hyun Koo from the Batista Lab at the Ragon Institute of Mass General Brigham MIT and Harvard in Cambridge Massachusetts. The approval of the malaria vaccines RTS,S/AS01 and R21/Matrix-M was a genuine landmark moment. Both present a portion of the Plasmodium falciparum circumsporozoite protein called PfCSP which contains an immunodominant major repeat region. The problem is this immunodominance may actually limit the immune response to other protective epitopes like the minor repeat and the junction region and this may be constraining vaccine efficacy and durability. Using B cell receptor knock-in mice the researchers found that the R21-included PfCSP epitope elicited robust B cell responses to the immunodominant major repeats but not to these other highly protective epitopes. They then defined a minimal peptide capable of eliciting minor repeat-specific B cell responses and generating highly protective antibodies. They characterized these antibodies bioinformatically and structurally to identify their protective traits which informed their design of improved immunogens. This is an elegant demonstration of how understanding the immunodominance hierarchy in a vaccine can guide rational improvements to get broader and more protective responses. Before we close out the episode today I want to briefly mention several additional papers that came across the desk this week without full abstracts available but they are worth knowing about. There is a retraction note in Nature Communications from August 6th on a paper by Yunzhi Wang from Fudan University in Shanghai titled Proteogenomics of diffuse gliomas reveal molecular subtypes associated with specific therapeutic targets and immune-evasion mechanisms. When a paper in this field gets retracted it is important to flag for the community. In Science from August 6th Maira Aguiar from the Basque Center for Applied Mathematics in Bilbao wrote a piece titled Dengue vaccines need long-term surveillance which is a timely call to action as dengue continues to spread globally. Nature published two notable short-form pieces this week. One by Max Kozlov titled COVID can wake up a slew of dormant viruses inside you from August 5th which connects COVID-19 infection to viral reactivation. The other by Edward Chen also from August 5th is titled First poo transplant to treat food allergy in people has exciting results which highlights early clinical results of fecal microbiota transplant as a strategy for food allergy which is a really novel application. There is an author correction in Nature Cell Biology from August 5th from Shuai Wang at Soochow University in Suzhou China on a paper about SARS-CoV-2 nucleocapsid protein and MAVS-mediated innate antiviral immunity. In EBioMedicine from August 5th Mihir Atreya from Cincinnati Children's Hospital Medical Center published a perspective titled Joint profiling of immune-endothelial cells in sepsis: promise, pitfalls, and the path forward which is relevant to the growing field of immune-vascular crosstalk in critical illness. In Gastroenterology from August 4th Rachele Frascatani from the University of Tor Vergata in Rome published a study titled Acquired Loss of IL-10 Function in Inflammatory Bowel Disease which touches on a really important immunoregulatory cytokine and gut disease. There is also an author correction in Nature Communications from August 3rd by Jiahui Zou from Huazhong Agricultural University in Wuhan on a paper about GGCX and its role in avian-like H1N1 swine influenza virus adaptation to interspecies receptor binding. And in PNAS from August 11th there is a retraction for a paper by Khan and colleagues on macrophage TBK1 signaling and breast cancer brain metastasis. Additionally there is a reply letter in PNAS from Sarah Rowe at the Department of Microbiology and Immunology at the University of North Carolina regarding antibiotic tolerance and clinical challenges in Klebsiella pneumoniae liver abscess. That is a wrap for this week on KodaKoda's Weekly Immunology News. What a remarkable week it has been. We had the pyrin inflammasome story landing three papers at once in Science Immunology which is the kind of convergent science that really moves a field forward. We had structural microbiology giving us atomic-level details of antibiotic resistance. We had tumor immunology papers showing us new ways that cancers hide from and resist immune attack and new engineering strategies to overcome those barriers. And we had vaccine science reminding us that even approved vaccines can be meaningfully improved when we understand the immunology more deeply. Thanks for listening and I will see you next week.