Welcome to KodaKoda's Weekly Immunology News, your weekly roundup of the latest research in immunology and microbiology. I am your host, and today we have a packed episode covering everything from HIV rebound dynamics to malaria vaccine breakthroughs, CAR-T cell therapy for brain tumors, and some fascinating new work on how our immune system shapes cancer, infection, and even the way viruses spread across continents. Let us get right into it.
We start today with a really important study published on July 7th 2026 in the Proceedings of the National Academy of Sciences. The first author is Mauro A Garcia from the Department of Medicine at Johns Hopkins University School of Medicine in Baltimore. The title is Inhibitory potential of autologous neutralizing antibodies sets quantitative limits on the rebound-competent HIV-1 reservoir.
So here is what they found. HIV cure requires preventing viral rebound after treatment interruption, but quantitative criteria defining the rebound-competent reservoir are lacking. The researchers studied individuals undergoing observational treatment interruption without confounding interventions to identify virologic and immunologic determinants of rebound. In 9 of 13 participants, rebound viruses were genetically identical or similar to proviruses in circulating resting CD4 positive T cells. They found no evidence of recombination among rebound sequences. Instead, resistance to autologous neutralizing antibodies, which they call aNAbs, was a critical determinant of viral rebound. Increased suppression of viral outgrowth by contemporaneous IgG isolated from plasma was correlated with longer time to rebound. Using something called inhibitory potential, or IP, defined as the log reduction in single-round infection at physiologic IgG concentrations, they were able to define quantitative limits governing rebound-competency with respect to contemporaneous aNAbs. Contemporaneous IgG antibodies inhibited different reservoir variants with a wide range of IP values from 0.4 to 8.2 logs, whereas rebound viruses were minimally inhibited, with values between 0.5 and 2.8 logs, indicating that inhibition by even up to 2.8 logs, which is 631-fold, cannot prevent rebound. Longitudinal analyses revealed that waning aNAb potency over time on antiretroviral therapy, or ART, allows previously neutralized variants to gain rebound potential, consistent with the finding that rebound can come from variants deposited in the reservoir at different pre-ART time points. So the key message here is that rebound competency is a dynamic, immune-governed property defined by quantitative immunologic constraints, including those exerted by aNAbs. This is really meaningful for anyone thinking about HIV cure strategies, because it tells us that the antibody threshold you need to maintain is not just high but has to be sustained over time.
Next up, also from the Proceedings of the National Academy of Sciences on July 7th 2026, we have a study titled Inferring epidemiological parameters under an infectious phylogeography model with visitor dynamics. The first author is Albert C Soewongsono from the Department of Biology at Washington University in St. Louis. This one sits at the intersection of epidemiology, evolutionary biology, and mathematical modeling.
During an outbreak, infectious disease can spread among populations through host movement, potentially fueling local outbreaks with their own epidemiological dynamics. However, it is difficult to know how often infections between populations are transmitted by diseased travelers infecting healthy residents when abroad, rather than by diseased residents infecting healthy travelers who later return home with the new pathogen. In this paper, the authors introduce a phylogeographic model where pathogens spread through visitor dynamics, whereby hosts visit other populations through short trips before returning home. They used the stationary properties of an epidemiological compartment model with visitor dynamics to construct an approximation that is statistically accurate and computationally tractable for phylogenetic modeling. They also derived mathematical properties for the approximating model that provide a sufficient condition under which the approximation remains accurate. They applied the model to empirical infection data and travel statistics from the European SARS-CoV-2 pandemic. Inference under their model suggests that in the early stages of the outbreak, SARS-CoV-2 was more often pulled into the home countries of returning travelers than pushed into foreign countries by visitors from abroad. Estimates of host movement-related parameter values under the visitor model suggest that alternative migration models with trips of indefinite length may underestimate the magnitude of outbreaks caused by visitors. The study emphasizes the importance of carefully incorporating host movement dynamics into epidemiological models. A great reminder that how people physically move around the world is as important as the biology of the pathogen itself.
Moving along, still in the Proceedings of the National Academy of Sciences from July 7th 2026, we have a study titled Fatty acid regulation and phosphatidylethanolamine biosynthesis are important for hepatitis E virus replication. The first author is Kush K Yadav from the Department of Animal Sciences at the College of Food Agricultural and Environmental Sciences in Wooster Ohio.
Hepatitis E virus, or HEV, is a leading cause of viral hepatitis globally and is associated with adverse outcomes during pregnancy. Despite its clinical significance, the mechanisms driving enhanced HEV replication during pregnancy remain poorly understood. In this study, the researchers uncovered a lipid-mediated pathway that facilitates HEV replication, with potential implications for pregnancy-associated pathogenesis. Lipidomic profiling reveals a marked upregulation of oleic acid during HEV infection in both human liver cells and in HEV-3ra-infected pregnant rabbits. They showed that oleic acid significantly enhances HEV replication, possibly through interaction with a predicted fatty acid-binding domain located within the papain-like cysteine protease region of the HEV ORF1 polyprotein. They further demonstrated that phosphatidylethanolamine, or PE, levels are elevated during HEV-3ra infection in pregnant rabbits, and that inhibition of PE biosynthesis by CRISPR/Cas9-mediated knockdown and silencing of phosphatidylserine decarboxylase and phosphoethanolamine cytidylyltransferase genes that are responsible for PE synthesis resulted in decreased HEV replication, indicating that PE is important for HEV replication. Additionally, they found that placental lactogen hormone, which is elevated during late pregnancy, stimulated fatty acid accumulation and potentiated HEV replication, therefore providing a potential explanation for pregnancy-associated adverse outcomes. Collectively, these findings reveal an important role of host lipid metabolism in HEV replication and offer mechanistic insights into lipid-dependent enhancement of HEV replication and a potential role of lipid reprogramming in HEV pathogenesis. The results may inform potential future anti-HEV therapeutic strategies targeting lipid pathways. Fascinating work, especially for anyone thinking about why pregnant women are so uniquely vulnerable to hepatitis E.
Now let us move over to Science, where we have several compelling papers this week. The first one was published on July 2nd 2026 and is titled Membrane protein solubilization and structure determination using de novo-designed proteins. The first author is Ljubica Mihaljević from the Department of Biochemistry at the Institute for Protein Design at the University of Washington in Seattle.
Developing therapies and vaccines against integral membrane proteins is hindered by their extensive hydrophobic surfaces, which complicate production and structural analysis. The authors describe a general deep learning-based design approach for solubilizing native membrane proteins while preserving their sequence, fold, active-site, and ligand-binding properties. Genetically encoded de novo proteins called WRAPs, which stands for water-soluble RFdiffused amphipathic proteins, surround the lipid-interacting hydrophobic surfaces, rendering them thermostable and water-soluble without the need for detergents. The researchers designed WRAPs for both monomeric and oligomeric beta-barrel outer membrane proteins and helical multipass transmembrane proteins. A 2.95-angstrom-resolution cryo-electron microscopy structure of WRAPed mycobacterial porin demonstrates that WRAPs can be used for the structural determination of membrane proteins in solution. And as a step toward syphilis vaccine development, they generated soluble versions of Treponema pallidum antigens. That last part is particularly exciting from a public health standpoint, as syphilis has been making a troubling comeback globally.
Also in Science from July 2nd 2026, there is a study titled ILC2s regulate a fibroblast progenitor niche in the pancreas. The first author is Thomas Yip from the University of Cambridge, specifically the CRUK Cambridge Institute.
Local fibroblast development and densities influence organ health and disease, although it remains unclear how tissue fibroblast topography is controlled in situ. The team defined Group 2 innate lymphoid cells, known as ILC2s, as key regulators of fibroblast homeostasis in the pancreas. ILC2s colocalized with fibroblasts expressing the genes Pi16, Dpp4, and Ly6c in an interstitial niche of the exocrine pancreas, which encapsulates the organ parenchyma. ILC2s specifically regulated the expansion of Pi16 Dpp4 Ly6c positive fibroblasts, which have progenitor capacity, while restraining differentiated intraparenchymal Col15a1 positive fibroblasts during inflammation. These circuits reinforced fibroblast numbers after injury and set an inflammatory threshold. The ILC2 and Pi16 Dpp4 Ly6c positive fibroblast progenitor niche expanded around tumors and controlled cancer-associated fibroblast ontogeny and density. So ILC2-fibroblast dialogue represents a regulatory node that locally orchestrates tissue homeostasis and pathology. This kind of crosstalk between innate lymphoid cells and stromal cells is an emerging theme in tissue immunology, and seeing it operate in the pancreas with implications for both inflammation and cancer is very significant.
Still in Science on July 2nd 2026, another paper caught my attention titled Surface immune signaling unlocks NLR activation through mRNA alternative splicing. The first author is Chuyun Gao from the State Key Laboratory of Agricultural and Forestry Biosecurity at Nanjing Agricultural University in China.
Plants activate pattern-triggered immunity and effector-triggered immunity to combat pathogens. However, how these systems coordinate immune activation while preventing autoimmunity remains poorly understood. In this study, the authors uncovered a regulatory mechanism in which surface immune signaling unlocks nucleotide-binding leucine-rich repeat, or NLR, immune receptor activation through mRNA splicing. They identified an N-terminal prodomain in the potato late blight resistance protein Rpi-vnt1.1 that inhibits resistosome formation, preventing potential autoactivation of this NLR. Upon pathogen perception, PTI signaling induced alternative splicing of Rpi-vnt1.1 mRNA, removing this inhibitory element. This primed Rpi-vnt1.1 for activation by the Phytophthora infestans effector AVRvnt1, enabling resistosome assembly and immune signaling. The widespread conservation of N-terminal extensions in coiled coil-type NLRs points to a common regulatory mechanism in preventing potential autoactivation while preserving pathogen sensitivity. Even if this is plant immunity, the conceptual parallels to how we think about immune checkpointing and autoimmunity in mammals are striking.
Also in Science on July 2nd 2026, we have a very compelling study titled A dietary switch promotes sensory neuron-dependent cancer-associated cachexia. The first author is Michael Cross from the Department of Pathology at New York University Grossman School of Medicine.
Sickness behaviors are common in cancer-associated cachexia and affect up to half of lung cancer patients. The researchers demonstrate that among the most common cancer mutations, loss of liver kinase B1, or Lkb1, promotes the development of cachexia in preclinical models of lung cancer. In an effort to improve caloric intake with an obesogenic high-fat diet, they paradoxically observed worsened cachexia-associated sickness. They found that local production of prostaglandin E2, rather than circulating factors, promotes sickness and that genetic, dietary, and pharmacological inhibition of tumor-derived prostaglandin E2 suppresses sickness and cachexia. Notably, they demonstrate that lung sensory neuron abrogation prevents prostaglandin E2-dependent cachexia. The study establishes localized tumor-derived signals to sensory neurons, rather than circulating factors, as drivers of cachexia and highlights a previously unknown role of the peripheral nervous system in cancer cachexia. This challenges the old view that cachexia is primarily driven by systemic cytokines floating around the blood, and instead points to a much more local, neurologically mediated process.
Now we head to Nature Medicine for a very important paper published on July 1st 2026. The title is Innate immune responsiveness predicts enhanced cellular immunity and symptomatic disease after controlled human influenza infection. The first author is Loukas Papargyris from the Department of Infectious Disease at Imperial College London.
Controlled human influenza infection studies can uniquely interrogate the early immune factors associated with clinical outcome. In this study, 27 healthy volunteers with low strain-specific serum neutralizing antibody levels were challenged with influenza A/H3N2 virus. Twenty-two became infected, with 18 developing mild-to-moderate symptoms and four remaining asymptomatic. Local and systemic immune profiling revealed innate pathways that engaged more rapidly and to a higher level in symptomatic participants. Earlier monocyte and dendritic cell activation correlated with higher symptom scores but also enhanced natural killer and CD8 positive T cell activation thereafter. At baseline, peripheral blood mononuclear cells from symptomatic participants were more responsive to in vitro challenge, indicating a predisposition to divergent immunological outcomes at the time of virus exposure that was subsequently modulated by infection. These results show that human innate cell responsiveness is a predeterminant of both symptomatic disease and cellular immune responses known to promote viral clearance, suggesting potential targets for therapeutic intervention if decoupled. This is a fascinating paradox. The very innate immune responsiveness that makes you sicker is also the thing that helps you clear the virus more effectively. The idea that you might be able to decouple those two outcomes therapeutically is a really exciting research direction.
Now to Nature, where we have two major papers on July 1st 2026. The first is titled Identification of cross-stage, cross-species malaria CD8 positive T cell antigens. The first author is Camila R R Barbosa from the Instituto René Rachou at Fundação Oswaldo Cruz in Belo Horizonte Brazil.
A major limitation on the development of a malaria vaccine is the lack of validated T cell epitope targets. Plasmodium falciparum is the most prevalent malaria parasite affecting humans in Africa, whereas Plasmodium vivax is more widespread and is the main species that causes malaria in the Americas and Asia. Plasmodium vivax exclusively infects peripheral-blood reticulocytes, which retain RNA and the capacity for host protein synthesis. The authors previously reported that reticulocytes infected with Plasmodium vivax express human leukocyte antigen class I, or HLA-I, which enables recognition and killing of the parasite by CD8 positive T cells. In this study they use immunopeptidomics to identify Plasmodium-antigen-derived peptides presented by HLA-I on infected reticulocytes. They identified 453 unique peptides mapping to 166 proteins. Seventy-five antigens were housekeeping proteins that are constitutively expressed at multiple stages of the parasite's life cycle and are highly conserved between Plasmodium species. Identical peptides were presented in different individuals by the same or distinct HLA-A, HLA-B, and HLA-C alleles, as well as by the non-classical HLA-E allele. The antigenicity of the newly identified epitopes was validated in samples from both Plasmodium vivax-infected and Plasmodium falciparum-infected individuals. Furthermore, T cell responses to several of these antigens were observed in the blood and liver of non-human primates after infection with Plasmodium or immunization with attenuated parasites. Two antigens also induced protective CD8 positive T cell-mediated immunity in rodents. These antigens thus have the potential for use in a cross-stage and cross-species malaria vaccine. That word cross-stage and cross-species is really the headline here. A vaccine that works across different life cycle stages and different Plasmodium species would be transformative for global malaria control.
The second major Nature paper from July 1st 2026 is titled Dual tumour-myeloid targeting of glioblastoma with GPNMB CAR-T cells. The first author is Neil Savage from the Department of Biochemistry and Biomedical Sciences at McMaster University in Hamilton Ontario Canada.
Glioblastoma is a lethal brain tumour for which current multimodal treatment rarely prevents recurrence. Therapeutic failure is driven by extensive intratumoural cellular heterogeneity with a microenvironment dominated by tumour-associated macrophages that sustain tumour growth and immunosuppression. Although chimeric antigen receptor, or CAR, T cell therapies are being developed for glioblastoma, sustained response has been undermined by non-uniform antigen expression, antigen loss, and microenvironmental barriers that are not directly engaged by tumour-targeting designs. These limitations motivated the authors to think about glioblastoma as a coupled tumour-immune system rather than a single malignant compartment. They used a multi-omic target discovery platform to identify GPNMB as a dual-compartment antigen in glioblastoma. Anti-GPNMB CAR-T cells showed potent anti-tumour activity, with long-term disease control in orthotopic patient-derived xenografts and syngeneic glioma models through concomitant depletion of GPNMB positive tumour cells and immunosuppressive myeloid populations. By collapsing tumour control and microenvironmental reprogramming, these findings provide a new strategy for antigen selection and targeting in heterogeneous, myeloid-rich solid cancers. This is a really elegant approach because instead of just targeting the tumor cells, you are simultaneously dismantling the immunosuppressive myeloid environment that protects the tumor. Two birds, one CAR-T cell.
Now let us go through several strong papers from Nature Communications published on July 1st 2026. First up is a study titled Pre-existing antibody and T cell responses to SaCas9, AsCas12a and CasΦ are comparable in naive individuals. The first author is Vijaya L Simhadri from the Division of Hemostasis at the Office of Plasma Protein Therapeutics at the Center for Biologics Evaluation and Research at the Food and Drug Administration in Silver Spring Maryland.
Cas9 proteins are derived from human pathogens and are immunogenic, thereby raising potential safety concerns and limiting clinical effectiveness when using Cas9 as a gene-editing tool. Cas orthologs developed from organisms not directly associated with human infections may thus be safer. The authors compared the immunogenicity risk of SaCas9, which is derived from the human pathogen Staphylococcus aureus, AsCas12a, derived from the human commensal Acidaminococcus sp., and CasΦ, derived from a bacteriophage called Biggiephage. Ex vivo and in vitro analyses show that SaCas9, AsCas12a, and CasΦ are recognized similarly by antibodies and T cells from unimmunized individuals. Using mass spectrometry to identify MHC-I-bound peptides, they find SaCas9, AsCas12a, and CasΦ peptides presented on 9 MHC-I proteins commonly found in the North American population. Their results indicate that AsCas12a and CasΦ do not present a less immunogenic alternative to Cas9, and underscore the need for systematic immunogenicity evaluation of all Cas proteins intended for clinical use. Important cautionary findings for the gene therapy field. You cannot assume that just because a Cas protein comes from a non-human pathogen source it will be better tolerated immunologically.
Next in Nature Communications from July 1st 2026, there is a paper titled Adjunctive ibuprofen in pre-extensively drug-resistant and extensively drug-resistant tuberculosis, a phase IIA open-label pilot clinical trial. The first author is Kaori L Fonseca from the Germans Trias i Pujol Research Institute in Badalona Catalonia Spain.
Drug-resistant tuberculosis remains a major global health challenge, and excessive inflammation may contribute to tissue damage and poor outcomes. The team conducted a phase IIA prospective open-label pilot trial evaluating adjunctive ibuprofen in adults with pulmonary pre-extensively drug-resistant or extensively drug-resistant tuberculosis in Georgia. Twenty-eight participants received individualized background anti-tuberculosis regimens alone or with ibuprofen 400 mg daily for 2 months and were followed for 6 months. The primary efficacy outcome was the proportion of participants showing clinical and/or microbiological benefit, assessed by sputum culture conversion, radiological evolution, and WHO-defined treatment outcomes. Secondary outcomes were safety and tolerability, health-related quality of life, and inflammatory and transcriptomic responses. Adding adjunctive ibuprofen did not improve month-2 sputum culture negativity, time to stable culture conversion, radiological evolution, or final treatment outcomes. Safety and tolerability were similar between groups. However, ibuprofen treatment was associated with numerically greater reductions in several blood-based inflammatory measures and in transcriptomic signature scores associated with poor tuberculosis outcomes. These findings are exploratory and do not demonstrate clinical benefit but indicate biological activity and support evaluation of anti-inflammatory host-directed therapies in larger controlled trials. So the anti-inflammatory signal is there, but it did not translate into clinical outcomes at this scale. Worth a larger trial.
Also from Nature Communications on July 1st 2026, there is a paper titled RNF2 mediates H2A ubiquitination to promote colitis via suppressing monocyte-macrophage transition in mice. The first author is Fanyi Meng from the Department of Gastroenterology and Hepatology at the General Hospital of Tianjin Medical University in China.
Monocyte-macrophage transition is dysregulated in inflammatory bowel disease. While polycomb repressive complexes are crucial for maintaining cellular identity, their specific roles in colitis are poorly defined. The researchers show that Ring finger protein 2, which is a core catalytic subunit of polycomb repressive complex 1, regulates the monocyte-macrophage transition during colitis. It is highly expressed in the immature colon and circulating monocytes during ulcerative colitis. Mice with myeloid-specific deficiency exhibited attenuated experimental colitis, restored monocyte and macrophage balance, and improved anti-tumor necrosis factor alpha efficacy. Mechanistically, Ring finger protein 2 represses Runt-related transcription factor 3 expression via histone H2A lysine 119 monoubiquitination. This disrupts the inhibition of the recombination signal-binding protein for the immunoglobulin kappa J region, the central activator of the Notch pathway, thereby exacerbating inflammation. Silencing of the axis markedly inhibited proinflammatory responses and regulated monocyte-macrophage transition. These findings reveal that Ring finger protein 2 disrupts the monocyte-macrophage transition during colitis, offering insights into colitis treatments.
Two more papers from Nature Communications on July 1st 2026 to cover. First, Targeting rapidly cycling receptors CD2 and CD7 increases nanoparticle delivery to primary CD4 positive T cells. The first author is Paula M Cevaal from the Department of Infectious Diseases at the University of Melbourne at The Peter Doherty Institute for Infection and Immunity.
T cells are critically important to many diseases but are traditionally difficult to transfect. The hypothesis was that delivery of therapeutic cargo to T cells can be improved by targeting nanoparticles to surface receptors that undergo rapid receptor-mediated endocytosis. Using an internalisation assay that labelled intracellular and surface proteins with different fluorophores, they found that CD2 and CD7 exhibit significantly higher internalisation than other T cell receptors such as CD3 or CD4. Targeting CD2 and CD7 improves nanoparticle internalisation by non-stimulated, primary CD4 positive T cells and enhances the specificity of association to CD4 positive T cells. Functionalising mRNA-lipid nanoparticles with antibodies targeting CD2 or CD7 enhances mRNA delivery to CD4 positive T cells in vitro. Importantly, targeting CD2 or CD7 enables efficient lipid nanoparticle-mediated delivery of mRNA to T cells in blood and lymphoid tissue in vivo, demonstrating that targeting T cell receptor endocytosis can enhance nanoparticle-mediated drug delivery to T cells. This has obvious implications for HIV gene therapy, CAR-T manufacturing, and other T cell-targeted interventions.
And finally from Nature Communications on July 1st 2026, Interferon-elicited lipoprotein metabolism in lung fibroblasts facilitates premetastatic niche formation. The first author is Jian Gao from the Department of Thoracic Surgery at Zhongshan Hospital, Fudan University in Shanghai China.
While premetastatic niche formation is known to affect primary tumor lung metastases, the role of lung stromal cells in this process remains unclear. Through multiomics sequencing, the team identifies interferon-regulated CD34 positive fibroblasts that reshape the immunosuppressive lung microenvironment via VLDLR-mediated lipoprotein metabolism activation. Increased lipoprotein uptake facilitates intracellular lipid accumulation, followed by CD155 expression in fibroblasts. CD155 positive fibroblasts strongly induce cytotoxic CD8 positive T cell and NK cell exhaustion, resulting in the formation of a premetastatic niche. The genetic disruption of the interferon-VLDLR-CD155 axis robustly reinstates immune surveillance and suppresses lung metastasis in multiple tumor models. Notably, interferon-based therapy is potentiated by specific silencing of the interferon response in fibroblasts or CD155 blockade. A remarkable finding that interferons, long celebrated as antiviral and antitumor agents, can paradoxically fuel the formation of a premetastatic niche through fibroblast reprogramming.
Before we wrap up, let us briefly touch on some papers that came out this week without abstracts but are absolutely worth flagging.
In Nature on July 1st 2026, Denise L Doolan has a piece titled Seeking universal malaria-vaccine targets, which likely reflects on the findings from the Barbosa paper we discussed earlier and the broader field of malaria vaccinology.
Also in Nature, there is a piece titled Ebola preparedness must start with ecosystems and before humans show symptoms by Mulatu Biru Shargie, from July 2026, which touches on ecological and zoonotic dimensions of Ebola preparedness.
Nature also has a news item on an AI tool that spots antibiotics that fight drug-resistant gonorrhoea, and another from Mohana Basu on an antibiotic cocktail made by soil bacteria that can kill superbugs. Both of these speak to the urgency of the antimicrobial resistance crisis and the creative directions researchers are taking.
In Nature Microbiology from July 2026, Atin Sharma from the journal itself writes about Voices of microbiome researchers in an artificial intelligence era, which sounds like a fascinating perspective piece on where the field is heading. Also in Nature Microbiology, Mercy M Olorunshola from the State University of New York at Binghamton has a paper on evolved phage cocktails that outsmart biofilm defences, and Lavinia Renzi from the Centro de Investigación Príncipe Felipe in Valencia writes about a phage takes the wheel. Sandra M Holmberg from Umeå University has a Nature Microbiology paper on fatty diets disrupting mucus-microbiome-metabolite interactions to increase intestinal lipid uptake, which ties in nicely with our hepatitis E and cachexia stories from today.
From Nature Immunology in July 2026, Bin Wang from Fudan University has a piece titled From vaccinology to immunology and back, progress and challenges. This is a journal we always include given its exclusive focus on immunology, and this sounds like a thought-provoking overview of the field. Also in Nature Immunology, there is a paper on why regulatory T cells fail to control inflammation in rheumatoid arthritis. Regulatory T cells are supposed to keep autoimmunity in check, so understanding their failure in rheumatoid arthritis is clinically very important.
From Science Immunology, a journal we always cover, there is an erratum for a research article titled Claudins interact with LILRB immune inhibitory receptors to promote myeloid immunosuppression in cancer, published June 26th 2026. Errata are important to note so the scientific record stays accurate.
In the Proceedings of the National Academy of Sciences from July 7th 2026, Oliver D Howes from the Department of Psychosis Studies at the Institute of Psychiatry Psychology and Neuroscience at King's College London has a piece titled Targets for disease modification in schizophrenia, new findings add to evidence for the involvement of the immune complement system. The complement system has been increasingly implicated in neuropsychiatric disease and this is a compelling area to watch.
Also from the Proceedings of the National Academy of Sciences from June 30th 2026, Claire D Kim from the Department of Neurosurgery at New York University Grossman School of Medicine has a paper titled Modeling autoimmune encephalitis with the human hippocampus. Autoimmune encephalitis is a devastating condition where the immune system attacks the brain, and developing better models to study it is crucial.
There is also an erratum in Science Translational Medicine from July 2026 for a research article titled Guanosine diphosphate-mannose suppresses homologous recombination repair and potentiates antitumor immunity in triple-negative breast cancer.
And finally, from Nature Immunology in July 2026, there is a paper on why regulatory T cells fail to control inflammation in rheumatoid arthritis, which we mentioned but want to emphasize again as a key read for anyone working in autoimmunity.
That is it for this week on KodaKoda's Weekly Immunology News. We covered HIV reservoir dynamics, malaria vaccine targets, CAR-T cells for glioblastoma, innate immune predisposition to influenza, hepatitis E and lipid metabolism, cancer cachexia and the nervous system, gene editing immunogenicity, tuberculosis host-directed therapy, and so much more. The breadth of work happening right now across immunology and microbiology is truly remarkable. Thank you so much for listening, and we will see you next week.