These data collectively establish FGL1/TACI as the negative regulator for the BAFF/APRIL/TACI “druggable universe”, and adding new B cell regulatory function of FGL1 beyond our early discovery of the FGL1/LAG-3 for T cell regulation.

Therefore, FGL1 does not compete with BAFF/APRIL binding but instead, negatively regulate TACI function through receptor endocytosis.

In this study we found FGL1 as the third (and the only inhibitory) ligand for TACI. We decoded the mysterious TACI N terminal 1-30 peptide as the unique FGL1 binding site which is totally different from the canonical BAFF/APRIL binding regions.

Huge appreciation to Lieping @YaleIBIO and Pascal Schneider @unil, and in particular @tina_t_su, who made tremendous contributions to this work. The TACI field was too cold during these years but resilience can made magic happen!

Online now: The liver-secreted protein FGL1 restrains a subset of innate-like B cell responses via the receptor TACI dlvr.it/TTn4Lx

My honor to host Ting Zhou from Westlake U. , my close friend and colleague while at Yale. I encouraged him to switch from structure to the immuno-oncology field. Look at him now…he is doing so well and even more immunology than me :)

My great pleasure to host Dr. Dario Vignali visiting NYU to present exciting data on LAG-3 immunotherapy and mechanisms with PD-1 combination.

My great pleasure to join the IV ASPIC-ASEICA @ASEICAnews conference to discuss our efforts in novel immunotherapies. See you at Santiago de compostela Spain in Nov.!

Super exciting talk from @geochurch @BioSpark_Group

It’s been six years! The journey has not been easy. Excited to see BioSpark is getting quite influential! Together, let’s Spark Biomedicine! @BioSpark_Group 2nd annual conference @MIT

Nice review from Ivan for innate and IFN lovers!

Check this out for all interferon lovers! An authoritative review on interferon biology by @Lo_Zanzi!

Anti-Siglec-15 Therapy Improves Bone Health in Osteogenesis Imperfecta Mice clinicaltrialvanguard.com/ne…

RT @Cathy7852375132: $NXTC: NC605 (anti-Siglec‑15 antibody) preclinical data released: NA605 significantly improved bone density, bone tiss…

🧬 BREAKING: Our CRISPR-GPT paper is out TODAY in Nature Biomedical Engineering @natBME ! 🤯 We built an AI agent that turns ANYONE into a gene-editing expert in 1 DAY instead of months. An undergrad with ZERO experience achieved 90%+ editing efficiency on their FIRST attempt. 🧵 Here's how we're building expert AI agents for cutting-edge biotechnology: 🎯 The Problem: CRISPR is revolutionary but requires PhD-level expertise, it can take weeks to learn, adopt, and design, analyze a CRISPR experiment for R&D or making life-saving medicine. Even Pro scientists can make small mistakes (e.g. typos in guideRNA or cloning design) that cost months to find out, slowing us down. 💡 Our Solution: CRISPR-GPT - an AI co-pilot from @Stanford @Princeton @GoogleDeepMind that guides you through EVERY step via simple conversation 🔬 Real Results: -Novice researcher: ~90% editing on 1st go -Training time: Months → 1 day -100% success rate in our trials -Even experts save days/weeks on data analysis & troubleshooting 🤖 How it works: Our multi-agent system handles: CRISPR system and delivery method selection, guideRNA design, Protocol generation, Real-time troubleshooting, Data analysis, and beyond. All through natural language! No coding, no complex software. 📊 We benchmarked it extensively: -288 evaluation scenarios/cases -Outperformed GPT-4o on ALL gene editing tasks -Trained on 11 years of expert discussions -Covers knockout, base-editing, prime-editing & epigenetic editing 🌍 Why this matters: -Every lab can now use CRISPR with an AI system distilling expert knowledge and skills. -Every student can learn faster. -Every researcher can tackle bigger challenges without worrying about small mistakes. -Customized CRISPR design can be automated based on your need and the context of R&D workflow. -Agentic AI ensure safety, privacy, and responsibility -We're not just automating gene editing - we're using AI to power scientists to cure diseases. 🚀 Try it yourself! Beta access available at: genomics.stanford.edu Paper: nature.com/articles/s41551-0… Code: github.com/cong-lab/crispr-g… Benchmark (companion work, Genome-bench): github.com/mingyin0312/RL4Ge… Co-first and key authors: @YuanhaoQ @KaixuanHuang1 @MingYin_0312 PIs: @lecong @MengdiWang10 Key collaborators: @Rbaltman @denny_zhou The future of biology and science is conversational. The future is now. @natBME @NaturePortfolio #CRISPR #AI #GeneEditing #Biotech #Science #AISafety

LAG-3 (lymphocyte-activation gene 3) is a signal/checkpoint found on the surface of T cells - the immune system’s frontline fighters. Learn more about LAG-3, the 3rd immune checkpoint to be clinically validated in melanoma, including emerging therapies & ongoing #clinicaltrials.

CINTER-seq enables in situ capture and multimodal profiling of interacting cells in living mice, uncovering specific LAG3-MHC II-mediated CD4+ T cell-cancer cell interactions & tumor-reprogrammed neutrophils cell.com/immunity/fulltext/S… @ImmunityCP

New #JITC review: Therapeutic potential of targeting LAG-3 in cancer bit.ly/4nHQO2h @diwakardavar @UPMCHillmanCC