Welcome to KodaKoda's Weekly Immunology News. I am so glad you are tuning in today because we have a packed episode full of fascinating science spanning cancer immunotherapy, innate immunity, virology, and even some microbiology discoveries that will genuinely surprise you. Let us dive right in.
We are starting with a big one from the world of cancer treatment. Published on July 16th 2026 in Nature Medicine, the paper is titled Englumafusp alfa plus glofitamab in B cell non-Hodgkin lymphoma a phase 1 trial. The first author is Martin Hutchings from Rigshospitalet and the University of Copenhagen in Denmark.
So here is the situation. B cell non-Hodgkin lymphoma, which we will call B-NHL, is a type of blood cancer, and when it comes back after treatment or stops responding to it, the options can be really limited. Doctors and patients desperately need effective therapies that are ready to go off the shelf without needing to be custom-made for each individual. This study tackled that problem head on.
The trial tested a drug called englumafusp alfa combined with another drug called glofitamab in patients with relapsed or refractory B-NHL. Now englumafusp alfa is what is called a CD19-4-1BBL co-stimulatory molecule. What that means is it is designed to give a kind of extra boost to immune cells, telling them to wake up and attack the cancer more effectively. Think of co-stimulation like a second ignition key that fully starts the immune engine. Glofitamab is a bispecific antibody that brings T cells right up to the cancer cells to kill them.
Before starting treatment, patients also received a drug called obinutuzumab to prepare the immune system. Then glofitamab was introduced with careful step-up dosing to manage side effects, followed by eleven cycles of glofitamab together with englumafusp alfa at escalating doses.
A total of 134 patients were enrolled. Among them 109 had aggressive B-NHL and 25 had what is called indolent B-NHL which is a slower-growing form. The good news on the safety front is that the maximum tolerated dose of englumafusp alfa was never actually reached, meaning they kept escalating without hitting an unacceptable ceiling of toxicity. There was one dose-limiting toxicity, which was a grade 5 Pneumocystis jirovecii pneumonia, a serious lung infection. Nearly all patients, 98.5 percent, had some adverse events, and grade 3 or 4 events occurred in about 59 percent, which is typical for this kind of intensive cancer treatment. Grade 5 events, meaning fatal ones, occurred in ten patients.
Now the efficacy results are where things get really interesting. In the group of patients with aggressive B-NHL who received englumafusp alfa starting on cycle 2 day 8, the overall response rate was 68.7 percent and the complete metabolic response rate was 56.6 percent. Among those who had never previously received chimeric antigen receptor T cell therapy, also known as CAR T therapy, the numbers were even better at 73.2 and 65.9 percent respectively. The study also found pharmacodynamic changes that confirmed englumafusp alfa was actually working in the way it was intended to, supporting its co-stimulatory mode of action. All in all, the authors conclude this combination shows encouraging efficacy along with a safety profile consistent with glofitamab monotherapy. Exciting early data for a challenging disease.
Next up we move into the world of structural immunology and receptor pharmacology. Published also on July 16th 2026 in Nature Communications, the paper is titled Mechanistic insight into signal bias by the agonist-dependent conformational dynamics of GPR84. The first author is Shota Suzuki from the Institute of Integrated Research at the Institute of Science Tokyo in Japan.
GPR84 is what is called an orphan class A GPCR, which stands for G protein-coupled receptor. The word orphan here just means scientists did not know its natural activating molecule for a long time. What makes GPR84 particularly relevant to our podcast is that it is primarily expressed in immune cells and plays important roles in inflammation and metabolism.
Using cryo-electron microscopy, which lets scientists visualize molecular structures at near-atomic resolution, the team determined the structure of GPR84 bound in complex with a G protein, activated by a biased agonist called DL-175. They also determined the structure of GPR84 in its inactive state bound to an antagonist called GLPG1205. Combined with signaling assays and molecular dynamics simulations, these structures mapped out the conformational landscape of GPR84 spanning from its inactive to its active state.
Here is the key finding. A molecule called DL-175 creates steric interactions, meaning physical blocking through molecular shape, with a specific residue called L336 6.52 on the receptor. This selectively prevents the conformational changes needed for beta-arrestin recruitment without interfering with G protein activation. In plain terms, the drug can turn on one signaling pathway in immune cells while leaving another off. This is what scientists call biased agonism. The practical takeaway is that these structural insights give drug designers a kind of molecular blueprint for creating GPR84-targeted therapeutics that can be precisely tuned to achieve specific effects in immune cells while minimizing unwanted side effects. Very elegant work.
Staying with innate immunity, let us move to a study from Nature Communications dated July 17th 2026. The title is ASB2 inhibits lipid accumulation to promote ILC1 homeostatic fitness and anti-tumor immunity in the mouse liver. The first author is Boqun Bao from the State Key Laboratory of Immune Response and Immunotherapy at the University of Science and Technology of China in Hefei.
Type 1 innate lymphoid cells, or ILC1s, are abundant in the adult liver and are really important players in immune surveillance, which is the immune system's ongoing patrol for abnormal or cancerous cells. Despite their importance, the molecular mechanisms that keep ILC1s alive and functional in the liver are not well understood.
The researchers re-analyzed published single-cell RNA sequencing data and found something notable, increased expression of a gene called Asb2 specifically in ILC1s from adult mouse livers. When they conditionally knocked out Asb2 in NKp46-positive cells, which targets ILC1s and NK cells, the mice showed impaired ILC1 survival and reduced numbers of these cells in the liver.
Using proteomics and bulk RNA sequencing, they found that ASB2-deficient ILC1s had enriched lipid metabolism pathways and increased lipid storage. When they pharmacologically blocked lipid synthesis, they could actually prevent the apoptosis, meaning the programmed cell death, of ASB2-deficient ILC1s in laboratory cultures. This was a real proof-of-concept moment.
In a mouse model of colorectal cancer liver metastasis, they found that ILC1s naturally accumulate more lipid when the liver is under tumor attack, and losing Asb2 made the metastasis worse. On the flip side, when they inhibited lipid accumulation in wild-type cancer-bearing mice, the animals lived longer, seemingly because ILC1-mediated anti-tumor immunity was boosted. So ASB2 acts as a kind of gatekeeper regulating lipid metabolism to keep ILC1s healthy and ready to fight tumors. This opens up a potential new angle for ILC1-based cancer therapies targeting liver tumors.
Our next paper is from Nature Communications as well, dated July 16th 2026, and it is titled The unfolded protein sensor IRE1 is essential for homeostatic dendritic cell maturation. The first author is Victor Bosteels from the Laboratory for ER Stress and Inflammation at the VIB Center for Inflammation Research in Ghent, Belgium.
Conventional type 1 dendritic cells, called cDC1s, are professional antigen presenting cells that play a critical role in the immune system. They undergo what is called homeostatic maturation when they engulf apoptotic cells, meaning cells that have died in an orderly, programmed way. This process is marked by the activation of a transcription factor called LXR-beta, which coordinates cholesterol efflux out of the cell and dampens interferon-stimulated gene expression.
This study identifies a new and essential player in this process, a sensor called IRE1. IRE1 is classically known as a sensor of the unfolded protein response, a cellular stress pathway that is triggered when proteins accumulate incorrectly in the endoplasmic reticulum. But here it is doing something different and surprising.
When IRE1 was deleted, cDC1s, but not cDC2s, the other major conventional dendritic cell type, showed impaired homeostatic maturation and survival. IRE1 activation in cDC1s depends on apoptotic cell uptake and the resulting cholesterol influx into the cell, which explains why IRE1 has such high baseline activity in these cells.
Crucially, instead of triggering a canonical unfolded protein response, IRE1 here activates a steady-state regulated decay program that degrades a microRNA called miR-92a-1. That microRNA would otherwise suppress a cholesterol-efflux transporter called Abcg1. So by degrading this microRNA, IRE1 allows the cell to pump cholesterol out more efficiently. Without IRE1, cDC1s cannot efflux cholesterol properly, and they die at higher rates. This death could be rescued by blocking microRNA synthesis or by treating the cells with reconstituted high-density lipoprotein. The paper establishes IRE1 as a cholesterol sensor in cDC1s and reveals a parallel pathway to LXR that maintains cholesterol homeostasis during dendritic cell maturation. Beautifully mechanistic work.
Let us shift gears and talk about a study with major implications for pandemic preparedness. Published in Nature Communications on July 16th 2026, the title is Triple IFN pathway deficiency sensitizes mice to human respiratory virus infection independent of human viral receptor expression. The first author is Qinghong Fan from the Guangzhou Key Laboratory of Clinical Pathogen Research for Infectious Diseases at Guangzhou Medical University in China.
Interferon pathways are the frontline innate immune barriers that most viruses encounter when they try to infect a host. Scientists have long known that partial deficiencies in these pathways can make humans or animals more susceptible to infection. But a key unknown was whether completely wiping out all three interferon pathways could make mice susceptible to human viruses even without expressing the specific human receptor those viruses normally need to enter cells.
To answer this, the team developed a mouse model called AGL, which stands for triple knockout of IFNAR, IFNGR, and IFNLR. Those are the receptors for type I, type II, and type III interferons respectively. By knocking out all three in one step, they created a mouse with severely compromised innate immunity.
The results were striking. These AGL mice became susceptible to a diverse set of human respiratory viruses including adenovirus type 55, which is a double-stranded DNA virus, human monkeypox virus clade IIb, also double-stranded DNA, parainfluenza virus which is a negative-sense single-stranded RNA virus, and the clinically isolated SARS-CoV-2 delta variant which is a positive-sense single-stranded RNA virus. The fact that these infections took hold without the mice expressing the typical human viral receptors suggests that interferon pathways, and particularly the type III IFN pathway, constitute a crucial backup antiviral defense layer. The authors also ran proof-of-concept antiviral drug studies with monkeypox and parainfluenza viruses, highlighting the translational value of this model. The AGL mouse could become a universal platform for studying both emerging and established viruses without needing a specially tailored mouse model for each one.
Here is an interesting one from the intersection of microbiology and agriculture. Published in Nature Communications on July 16th 2026, the paper is titled Alginate foraging is conserved in geographically and taxonomically distinct ruminant microbiomes. The first author is Jeffrey Tingley from the Lethbridge Research and Development Centre at Agriculture and Agri-Food Canada.
Seaweed is gaining a lot of attention as a sustainable biomass resource with applications in biofuel, human nutrition, and animal feed. But how seaweed actually gets digested in the rumen of livestock has largely been a mystery. The rumen is the first and largest stomach compartment of ruminants like cows and sheep, and it is packed with a complex microbial community that breaks down plant material.
The team focused on the brown alga Saccharina latissima and investigated how it is catabolized within the rumen ecosystem of two different ruminant species. They used a combination of animal models, bacterial imaging, multilayered meta-omics analyses, and enzyme biochemistry. The striking finding was that geographically distinct ruminants harbor what are called conserved alginate utilization loci, meaning that the genetic machinery for breaking down alginate, the main structural polysaccharide in brown seaweed, is preserved across ruminant microbiomes regardless of where in the world those animals live.
Core enzymes involved in alginate metabolism have been maintained across populations, while some ancillary enzymes appear to be gained or lost through gene duplication or loss events. This conservation indicates that the ruminant microbiome retains a latent capacity to metabolize marine polysaccharides even in animals that have never encountered seaweed. Fascinating from an evolutionary perspective, and potentially very useful for making seaweed a viable and digestible feed supplement for livestock.
Moving on, we have a paper from Nature Communications dated July 16th 2026 titled The minor spliceosome component U4atac regulates JAK/STAT signaling to modulate hematopoiesis and immune responses in Drosophila melanogaster. The first author is Dania Shikara from the Department of Microbiology and Immunology at Dalhousie University in Halifax, Canada.
This one connects a rare developmental disorder to core immunological pathways through elegant genetics. The small nuclear RNA U4atac is a core component of the minor spliceosome, which is a molecular machine responsible for a specific subset of RNA splicing events in cells. In humans, mutations in U4atac cause rare developmental disorders including Roifman syndrome, which is characterized by growth restriction, brain anomalies, and immune deficiency.
To understand what goes wrong mechanistically, the researchers created a Drosophila, that is fruit fly, mutant with CRISPR-Cas9-induced mutations in U4atac. These mutant flies showed growth and neurodevelopmental defects, immunodeficiency, and gastrointestinal symptoms, mirroring the human syndrome. Through bulk RNA sequencing and functional assays, the team found that U4atac mutations affect the splicing of a large set of transcripts involved in innate immunity, hematopoiesis, and intestinal cell functions.
A particularly important target was the Drosophila Janus kinase homolog called hopscotch, or Hop. U4atac deficiency reduced Hop expression and caused hematopoietic defects, meaning defects in blood cell formation, at both the embryonic and larval stages. Crucially, the authors also found reduced expression of JAK1 and attenuated JAK/STAT signaling activation in patients with Roifman syndrome. JAK/STAT is an incredibly important signaling pathway in immunity and hematopoiesis. This work identifies disrupted Jak signaling as part of the pathogenesis of what is being called RNU4atac-opathy, which is a potentially actionable insight for future therapeutic development.
Now for a big metagenomics study. Published in Nature Communications on July 16th 2026, the paper is titled Diversity and distinctive characteristics of the global RNA virome in urban and peri-urban environments. The first author is Zihao Gao from the Center for Bioinformatics and Computational Biology at East China Normal University in Shanghai.
RNA viruses are everywhere, and they are intimately linked to human health. But the ecology of environmental RNA viruses, meaning how they distribute and function in the environments where humans live and work, is deeply underexplored. This study aimed to change that in a big way.
The researchers analyzed 2922 metatranscriptomic samples from urban and surrounding environments including transit hubs, hospitals, and banks, alongside peri-urban settings, spanning 102 cities across 31 countries. From this enormous dataset they constructed what they call the Urban and Peri-urban RNA Virus Atlas, or UPVAtlas, containing 54,945 RNA viruses, 77 percent of which had never been previously observed. That is an extraordinary expansion of our knowledge of viral diversity.
Phylogenetic reconstruction based on RNA-dependent RNA polymerases from UPVAtlas greatly expanded the evolutionary diversity of known RNA viruses, leading to the identification of two potential candidate phyla, one candidate class, and several previously unclassified evolutionary clades. Host association analyses revealed the ecological complexity of environmental RNA viruses, with diverse vertebrate-related and what are called ESKAPE pathogen-related viruses, ESKAPE being a group of particularly problematic bacteria and their associated phages, underscoring the need for continued monitoring of urban environments to track RNA viral prevalence and dynamics. This work has direct relevance to future public health surveillance and pandemic preparedness.
Now here is a study right at the intersection of DNA damage, cancer biology, and immunology. Published in Gastroenterology on July 16th 2026, the title is A DR5/Ligase 3-mediated feedback loop perpetuates immunogenicity in mismatch repair deficient colorectal cancer. The first author is Suisui Hao from the Department of Medicine at the Keck School of Medicine of the University of Southern California.
Colorectal cancers with deficient DNA mismatch repair, abbreviated dMMR, and a condition called microsatellite instability or MSI, are generally thought to be intrinsically immunogenic, meaning the immune system more readily recognizes and attacks them. This is why they tend to respond better to immune checkpoint inhibitor therapy. But here is the problem: a significant fraction of dMMR/MSI colorectal cancers do not respond or eventually become resistant to these checkpoint inhibitors, and the underlying mechanisms have been unclear.
Using transplant syngeneic tumor models, immune cell co-culture assays, and air-liquid interface culture of tumor-derived organoids, the researchers found that inactivating a gene called Mlh1, which is part of the mismatch repair machinery, causes endoplasmic reticulum stress and subsequent death receptor 5 or Dr5-mediated apoptosis in colorectal tumor cells. That apoptosis then gets amplified by a nuclear protein called Ligase 3 or Lig3, which mediates the release of extrachromosomal circular DNAs, called eccDNAs, from the dying tumor cells.
These eccDNAs act as damage-associated molecular patterns that further stimulate immune cell activation. A feedback loop between Dr5 and Lig3 perpetuates both apoptosis and immune activation in Mlh1-deficient tumors. In mice, this feedback mechanism was critical for the response to immune checkpoint inhibitor therapy, and the clinical relevance was supported by a significant association between DR5 or LIG3 expression and the efficacy of checkpoint inhibitor therapy in human cancer patients. This finding reveals a functional link between deficient mismatch repair and anti-tumor immunity, and could offer new biomarkers or combination strategies for improving checkpoint immunotherapy.
Let us look at hematopoietic aging now. Published in Cell Stem Cell on July 16th 2026, the paper is titled Vitamin C attenuates primate bone marrow aging at the molecular and progenitor level. The first author is Yanxia Ye from the State Key Laboratory of Organ Regeneration and Reconstruction at the Institute of Zoology, Chinese Academy of Sciences in Beijing.
Bone marrow aging leads to impaired hematopoiesis, which is the production of blood cells, and compromised immunity. This is a well-documented problem in older people, but whether it can be modified in primates has not been explored at the single-cell level until now.
Using single-cell transcriptomics, the researchers mapped the landscape of primate bone marrow aging and then asked a fascinating question: what does long-term oral vitamin C supplementation actually do to aging bone marrow at the molecular level? They found that aging drives severe depletion of common lymphoid progenitors, which are the precursors to lymphocytes including B cells and T cells, along with a myeloid-biased output from hematopoietic stem and progenitor cells, meaning older marrow tends to favor producing innate immune and myeloid cells over lymphocytes. Vitamin C administration partially offset these phenotypes by expanding the common lymphoid progenitor pool and rebalancing lineage commitment trajectories.
This corresponded to an approximately four-year reduction in transcriptomic age estimates, which was cross-validated using an epigenetic clock. Cell-cell communication analyses revealed that vitamin C remodels intercellular signaling, with a particular spotlight on a candidate pathway linked to progranulin, a growth factor signaling protein abbreviated GRN. Human in vitro assays further showed that recombinant progranulin could mimic selected vitamin C-associated molecular actions. These findings delineate the molecular architecture of primate bone marrow aging and nominate potentially modifiable pathways for investigation in future interventional studies.
Now into the microbiology of phage defense. Published in Cell Host and Microbe on July 16th 2026, the paper is titled Gabija restricts phage circularization and DNA replication. The first author is Alex Hong from the Department of Microbiology and Immunology at UC San Francisco.
Bacteria have evolved sophisticated defense systems against bacteriophages, those viruses that infect bacteria. Famous examples include restriction-modification systems and CRISPR-Cas. But another system called Gabija, which is a highly prevalent nuclease-helicase antiphage system, has remained mechanistically mysterious, particularly in terms of how it distinguishes self from non-self DNA.
This study reveals how Gabija works. The key insight is that phage-encoded DNA end-binding proteins that normally antagonize a bacterial complex called RecBCD sensitize phages to Gabija. When Gabija was tested in Pseudomonas aeruginosa against a temperate lambda-like phage, it was found to prevent phage genome circularization and subsequent replication.
DNA end-binding complexes, including a phage exonuclease and a single-stranded DNA annealing protein, as well as GamMu dimers that block the host repair complex RecBCD from loading onto DNA ends, were found to be necessary and sufficient to make phages and even plasmids sensitive to Gabija. Mutant phages that evolved to escape Gabija did so by losing these DNA end-binding proteins, which then allowed RecBCD to translocate on the DNA and protect those phages from Gabija. On the bacterial chromosome, RecBCD activity following any linearization event similarly prevents Gabija from targeting bacterial self-DNA. So the self versus non-self discrimination mechanism is elegant: Gabija attacks linear DNA that lacks RecBCD activity, which marks the DNA as foreign.
We also have a spectacular methods paper. Published in Cell on July 16th 2026, the paper is titled Spatial proximity sequencing maps developmental dynamics in the germinal center. The first author is Huili Wang from the Pritzker School of Molecular Engineering at the University of Chicago.
The germinal center is a specialized structure in lymphoid tissues where B cells undergo rapid proliferation, mutation, and selection to produce high-affinity antibodies. Understanding the complex cellular dynamics within germinal centers is a central goal of modern immunology.
This paper introduces a technology called Sprox-seq, which stands for spatial proximity sequencing. It allows simultaneous profiling of surface proteins, protein complexes, and mRNAs, all while recording the spatial tissue location of each molecule. The team profiled 32 proteins, 528 pairwise protein interactions, and thousands of mRNAs across human tonsil tissue including germinal centers.
Mapping tissue-wide protein interactions recapitulated the RNA-defined tissue architecture but also revealed higher interaction complexity in the light zone of the germinal center. Protein interaction trajectories uncovered a B cell state transition that was distinct from what you would predict from RNA data alone. Integrated protein complex and mRNA analysis connected spatially enriched complexes with mitotic pathways. Sprox-seq also captured cell-cell interactions, such as those between B cells and follicular dendritic cells mediated by the receptor complex VLA-4 and VCAM1. This is a genuinely powerful new tool for multi-modal spatial immunology.
Now here is an important clinical and epidemiological study. Published in EBioMedicine on July 16th 2026, the paper is titled Autoantibodies against type I interferons in patients with zoonotic H7N9 influenza an observational case-control study. The first author is Yongkun Chen from the Guangdong Provincial Key Laboratory of Infection Immunity and Inflammation at Shenzhen University Medical School.
Most birds carry avian influenza A viruses without getting severely ill, but when those viruses jump to humans, known as a zoonotic infection, they can be devastating. The H7N9 subtype of avian influenza has caused significant outbreaks in China. The question this paper asks is: why do some people become infected while others with similar exposure do not?
The authors hypothesized that autoantibodies that neutralize type I interferons might predispose people to H7N9 infection, similar to how loss-of-function mutations in antiviral factors have been linked to susceptibility. They screened serum samples from 199 Chinese patients with laboratory-confirmed H7N9 infection and 531 healthy uninfected controls, including poultry workers and close contacts, using a multiplex bead-based assay for IgG autoantibodies against IFNα2, IFNβ1b, and IFNω. Positive samples were then tested for IFN-neutralizing activity in a reporter assay.
The results were striking. Neutralizing autoantibodies against at least one type I interferon were detected in 19.1 percent of H7N9 patients but in only 1.1 percent of controls. Most patient sera targeted IFNα2 and/or IFNω. The presence of these neutralizing autoantibodies was associated with 8.2- to 25.3-fold higher odds of H7N9 infection. Autoantibody prevalence increased significantly with age, with 44.8 percent of patients 70 years or older carrying these autoantibodies. All selected sera with neutralizing autoantibodies blocked IFNα2-induced antiviral activity in cell culture. The authors suggest that screening for anti-type-I-interferon autoantibodies could be integrated into surveillance or targeted testing in environments with increased exposure to zoonotic influenza viruses, including potentially H5N1, the panzootic strain of current global concern.
Before we close out today, let me briefly touch on several papers that were published without full abstracts that are worth knowing about.
Nature published a news piece by Max Kozlov titled Explosive diarrhoea outbreak grips US how researchers are hunting its source, covering an ongoing investigation into a gastrointestinal illness outbreak, very relevant to public health microbiology.
From Nature Microbiology, a fascinating study titled Bacillus subtilis cells can escape biofilms by producing a hydrogel that ejects them, which explores how bacteria self-regulate their own biofilm community dynamics.
From Nature Immunology, a commentary by George Hajishengallis from Penn Dental Medicine at the University of Pennsylvania titled Innate immunity at the crossroads of protection and pathology insights from the Aegean, which reflects on fundamental questions in innate immunology. Given that this comes from Nature Immunology, a top-tier immunology journal, it is definitely worth seeking out.
From Nature Medicine, a news piece by Karen O'Leary titled Mining antigens for a universal malaria vaccine, touching on the ongoing global effort to develop broadly protective malaria vaccines.
Also in Nature, Flora Graham's Daily Briefing asks Can regrowing the thymus slow down ageing, which connects directly to adaptive immunity since the thymus is where T cells mature and its involution with age is a core driver of immune decline.
Rachel Fieldhouse also writes in Nature with a piece titled Biologists pinpoint how common virus triggers multiple sclerosis, which relates to a long-standing question about how Epstein-Barr virus may initiate the autoimmune cascade that leads to multiple sclerosis.
In Gastroenterology, Kupcinskas Juozas from the Lithuanian University of Health Sciences published a piece titled Finding the Signal in the Noise Can Fecal Microbiota Transplantation Deliver for Irritable Bowel Syndrome, which addresses the evolving evidence for microbiome-based therapies.
In Cell Metabolism, Fan Yang published a paper titled Ferroptosis heterogeneity in triple-negative breast cancer reveals an innovative immunotherapy combination strategy. Ferroptosis is an iron-dependent form of regulated cell death, and its intersection with tumor immunotherapy is an exciting emerging area.
There are also a couple of author corrections this week from Nature Communications regarding SARS-CoV-2 spillover potential in North American cervids, and from Nature Communications regarding molecular mechanisms of receptor recognition and antibody neutralization of coxsackievirus A6, as well as an author correction from Nature Medicine on integrated community-based HIV and sexual and reproductive health services for youth. And there is an expression of concern from the Proceedings of the National Academy of Sciences regarding a paper on Mycobacterium tuberculosis and mesenchymal stem cells, which the scientific community will want to follow.
And finally, there was an article title that was unfortunately cut off in our source materials, so we could not cover it fully this week, but we will keep an eye out for it.
That is a wrap on this week's KodaKoda's Weekly Immunology News. We covered cancer immunotherapy, innate lymphoid cells, dendritic cell biology, viral infection models, microbiome research, phage defense systems, spatial multi-omics in germinal centers, and autoantibody-mediated susceptibility to avian influenza. What a week for immunology and microbiology. Thank you so much for listening, and we will see you next week with another fresh batch of science.