Engineered CAR-T cells induce long-lasting remission in rheumatoid arthritis with a single infusion
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Updates every hour. Last Updated: 23-Jun-2026 23:16 ET (24-Jun-2026 03:16 GMT/UTC)
Rheumatoid arthritis (RA) affects an estimated 18 million people worldwide, and current anti-TNF biologics, such as adalimumab, require injections every two weeks, often for years or decades, frequently losing efficacy as anti-drug antibodies accumulate. Researchers at Tsinghua University have now engineered a novel class of CAR-T cells that specifically capture and degrade soluble tumor necrosis factor (TNF) through receptor-mediated endocytosis. By incorporating the TNFR1 ectodomain as the antigen-binding domain and applying CRISPR-mediated knockout of BCOR and ZC3H12A, the resulting TNFR1TIF cells expanded robustly and persisted for over one year in immunocompetent mice without any lymphodepleting preconditioning. A single infusion reduced serum human TNF to near wild-type levels and conferred long-term remission in a mouse model of RA, matching the efficacy of repeated high-dose adalimumab. This work establishes a host-machinery-independent, durable cellular targeted protein degradation platform for chronic inflammatory disease.
In a paper published in Mycology, a study of fungal diversity in the Gaoligong Mountains of southwestern China discovered ten new species of Inocybe and reported one species as a new record for China. Based on detailed morphological observations and combined ITS-LSU-rpb2 phylogenetic analyses, the study resolved the systematic positions of these taxa and recognized six major lineages within the genus. As an ecologically important ectomycorrhizal group, Inocybe plays a key role in forest ecosystems, while many species also contain toxic compounds that may cause poisoning in humans or animals. This work provides important taxonomic evidence for understanding the species diversity of Inocybe in China and highlights the Gaoligong Mountains as an underexplored hotspot of fungal diversity.
Human metapneumovirus (hMPV) is a prevalent respiratory pathogen without approved vaccines or targeted treatments. Researchers have discovered that hMPV’s regulatory protein M2-2 directly interacts with host splicing factors hnRNP H1, hnRNP M, and hnRNP U, thereby modulating the alternative splicing of cellular genes such as STRAP and TANC2. These splicing changes are essential for efficient viral protein production and infectious particle generation, with CRISPR knockout studies showing significant reductions in viral replication. Comparative analysis with other respiratory viruses reveals that this splicing modulation is highly specific to hMPV, highlighting a unique virus-host strategy. Targeting the M2-2–spliceosome interaction could offer a promising therapeutic approach.
A research team from the Institute of Aging and Regenerative Medicine at Jinan University, China, has examined how aging and disease are connected by exploring the aging-related remodeling of chromatin architecture. This study of chromatin architecture, the three-dimensional organization of DNA, gives scientists a better understanding of aging and its underlying mechanisms. Their review is published in Aging Research on May 8, 2026.
While multidrug-resistant Candida auris poses a global threat to public health, the impact and mechanism of drug resistance on fungal virulence remain unclear. This study reveals that fluconazole-resistant C. auris exhibits enhanced fitness and resistance to macrophage killing under zinc deficiency by mobilizing intracellular zinc. The inhibition of gene encoding Zn(II)2Cys6 transcription factor 4 (ZCF4) contributes to C. auris resistance to macrophage killing by suppressing the PI3K-AKT- mTOR pathway and downstream matrix metalloproteinase-9 (MMP-9) activity. Dietary zinc deficiency promotes the virulence of fluconazole-resistant C. auris. This research provides a mechanistic understanding of host-fungal interactions and highlights zinc intervention as a potential nutrient intervention strategy against fungal infection.