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Jia Ming Nickolas Teo et al.
Metabolic dysfunction-associated steatohepatitis hepatocellular carcinoma is particularly resistant toward immunotherapies. Through a multipronged approach integrating databases consisting of over 1,000 HCC patients and multiple murine HCC models, we identified SiglecFhi TANs-derived TGFβ as the key driver of their immune evasion and ICB therapy resistance.
Article
Shuo Ru et al.
The accumulation of RNA lariats in human DBR1-deficient cells impairs stress granule assembly–mediated PKR activation, and thereby cell-intrinsic antiviral immunity. Cells and brain samples from Dbr1Y17H/Y17H mice exhibit similar phenotypes. These findings provide a molecular mechanism by which human-inherited DBR1 deficiency underlies brainstem viral infections.
Brief Definitive Report
Arja Ray et al.
Specifically depleting CD206-expressing TAMs using a novel mouse model demonstrates the role of these macrophages in recruiting a tumor-reactive network of CD8 T cells, cDC1s, and NK cells.
Article
Tasia D. Kellogg et al.
The microbial metabolite succinate promotes tuft cell hyperplasia, which enhances the gut’s ability to protect against intestinal infections. This study reveals that microbiome-driven tuft cells’ hyperplasia in the colon helps defend against Clostridioides difficile infection, providing a pathway through which host and microbial interactions protect against pathogens. Succinate-producing bacteria improve survival in infected mice, and this protective effect is dependent on the presence of tuft cells, as evidenced by the lack of protection in tuft cells–deficient mice.
Article
Jida Huang et al.
This study reveals an underlying mechanism that mediates the rapid release of cytokines by ILC3s. Upon stimulation, the p38α–eIF6–Nsun2 axis rapidly promotes the nuclear export of cytokine mRNA in ILC3s, thereby maintaining intestinal homeostasis.
Article
Camila Robles-Oteíza et al.
Understanding mechanisms driving tumor escape during immune checkpoint inhibition is essential to combat acquired resistance. This study identifies hypoxia as a key feature of immune checkpoint inhibitor-resistant tumors and demonstrates that therapeutically targeting tumor hypoxia can delay acquired resistance.
Article
Evangelos Bellos et al.
Bellos et al. identify an enrichment of rare, damaging variants in BTNL8 in MIS-C patients. These variants result in impaired Vγ4+ γδ T cell engagement associated with altered gut homeostasis, which may contribute to the pathogenesis of MIS-C.
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Current Issue
Volume 221,
Issue 12,
2 December 2024
Reviews & Opinions
People & Ideas
Montserrat Cols
Professor Cindy Ma heads the Human Immune Disorders Laboratory at the Garvan Institute of Medical Research. She is a member of the Garvan Faculty, holds a conjoint appointment with UNSW Sydney (School of Clinical Medicine, Faculty of Medicine and Health), and is an NHMRC of Australia Investigator Grant Fellow (L1).
People & Ideas
Montserrat Cols
Professor Kazuyo Moro, D.D.S., PhD, finished her doctorate in the Department of Microbiology and Immunology at Keio University School of Medicine in 2007 and then worked there as a postdoctoral fellow for 5 years. She transferred to RIKEN Center for Integrative Medical Sciences (IMS) in 2012. For the first 2 years, she worked in the Laboratory for Immune Cell Systems as a senior researcher, and in 2015, she became team leader for the Laboratory for Innate Immune Systems. Since 2019, Prof. Moro holds dual appointments at RIKEN IMS and at Osaka University Graduate School of Medicine.
Review | Cancer Focus
Stefano M. Cirigliano, Howard A. Fine
Cirigliano and Fine explore the past, present, and future of glioma modeling, identifying limitations in current models and proposing new approaches integrating bioengineering and artificial intelligence. These innovations aim to better capture tumor heterogeneity and human brain microenvironment, enhancing therapeutic relevance and clinical translatability.

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