FrezzaLab

This is a topic I am very passionate about, and something I am learning every day. I hope you will enjoy the read, and you will find it useful. Happy to hear your views about the topic. The mindful scientist network.febs.org/posts/the-mind… #FEBSnet

💡Exciting news! Our latest study, in collaboration with Prof. Mirela Kuka’s lab, is out now—uncovering how T cell–derived IFN-γ can suppress T follicular helper (TFH) cells and limit antibody responses. 🚀🧵(1/10) embopress.org/doi/full/10.10… 🔬Approach: We used a subcutaneous LCMV infection model, tracking virus-specific CD4⁺ T cells. Surprisingly, we found two T-bet⁺ subsets—one producing granzyme B (GzmB) and another expressing Tcf-1, the latter being a TFHprecursor. (2/10) 🌟Key Finding: IFN-γ from T cells drives the TH1 fate and blocks TFHmaturation. When we blocked IFN-γ early, Tcf-1⁺ “precursor” cells fully developed into TFH, boosting germinal center B cells and antibody responses. (3/10) 📊Mechanism: Rather than acting solely via an “autocrine loop,” IFN-γ shapes the microenvironment by acting on other immune cells—likely dendritic cells—thereby steering CD4⁺ T cells toward a TH1-dominant response at the expense of TFH. (4/10) 📌Infections & Vaccines: We also tested other settings—like systemic infections or even MPLA-based immunizations—and consistently observed that reducing IFN-γ can enhance TFH and humoral immunity. Timing is critical for optimal effect. (5/10) 🧬Broader Impact: Our data help explain why some infections trigger robust TH1activity but limited antibody responses, and highlight how precisely timed IFN-γ modulation could improve immunization strategies. (6/10) 🔑Clinical Relevance: In severe or chronic viral infections, TH1-skewed responses can sometimes block high-affinity antibody production. Targeted IFN-γ blockade might tip the balance toward TFH, aiding pathogen clearance or vaccine success. (7/10) 💡Mechanistic Insights: By tuning IFN-γ signals, we can reprogram local lymph nodes and “unlock” TFH potential. This points toward new avenues to combine T cell and B cell–focused therapies for more effective vaccines. (8/10) 👏Huge congratulations to Mirela Kuka, Eleonora Sala, Maria Nelli and all contributors who co-led the study! (9/10) 📖Dive deeper into our research and its implications for antiviral defense and vaccines. We look forward to your thoughts and questions! Full paper here: embopress.org/doi/full/10.10… @SanRaffaeleMI @MyUniSR @ERC_Research @AIRC_it @EMBO @ArmeniseHarvard (10/10) 💬📚

@PLeippe yes! a significant one.

@FrezzaLab Agreed! Do you have a "starter pack" for the other platform for which accounts to follow for metabolism content?

This is a huge decision from the Guardian. I believe too that X has become a polarised political platform that has lost its purpose and sadly, I no longer support it, despite its initial good intention. I will move my activity to @frezzalab.bsky.social theguardian.com/media/2024/nov…

@shanmugamlab thanks! I am on bluesky

@FrezzaLab I enjoy following your posts. Where are u moving to?

I know firsthand that every platform reaching a certain critical mass will suffer from this issue (as you said, FB, for example), but I don't feel I can support X anymore. Your suggestion is valid, and it is what I tried to do for years here, but if the attacks on science are from people whose only intention is to discredit it, the discussion is no longer balanced, and science will overall lose.

All fair and I wish you the best Every platform is going to ‘suffer’ from the same issues on one side or the other. My take- do the best damn science- let people attack it so you can make it even better… and advance the understanding of health and biology for the betterment of all :)

@eric_novack @heniek_htw @elonmusk In fact, I left Facebook many years ago and transitioned to Twitter because of that problem. But again, this is not about political views (I never expressed any here).

Absolutely - your choice Can you blame @elonmusk ? He’s been subject to endless lawfare for years (not to mention the bureaucracy actively looking to see SpaceX fail and hindering for no reason) When Zuckerberg spent $400M in 2020 promoting Dems, that was ok though? R u on FB? I’m not attacking you- I’m truly trying to understand the mentality that has scientists actively reducing their reach

This is not about X being polarised (I have survived it for years); it is about how its owner is now using it as a pure political means. I don't have a sense of academic self-superiority; I just don't like how this platform is and will be exploited. I believe we are entitled to decide

lol- when it was suppressing viewpoints, it was not polarized Now that it is not It is polarized Science^tm is as infected by politics (and has been) as any area— but likes to hide under the blanket of academic self-superiority To @FrezzaLab and others- just get over yourselves, do science that amazes us and advances humanity - leave your politics out of it Thank you for coming to my TEDtalk

@A_Amunts For me, the problem is not with the algorithms or X itself, but how polarising protagonists use and exploit it. I realised this even more now that our dear Elon has decided to meddle with foreign politics. I find this very dangerous.

#Circadian disruption in #cancer hallmarks: Novel insight into the molecular mechanisms of tumorigenesis and cancer treatment sciencedirect.com/science/articl…

🥳 Happy to share our new preprint where we describe the molecular machinery regulating iron transport between lysosomes and mitochondria, how it controls the melanoma drug tolerant persister state and the consequences of its perturbation on ferroptosis 👉 researchsquare.com/article/rs-534…

Today in @CellCellPress we report a new pathway of ketone metabolism. This BHB shunt generates an orphan family of anorexigenic ketone metabolites that are chemical cousins of exercise-inducible Lac-Phe. Congratulations @mariadolores_mg @Stanford_ChEMH cell.com/cell/fulltext/…

Fantastic opportunity to work with a great mentor on a very fascinating topic! 🔥🔥🔥

@SdelciL @NatureComms @NataliaPardoL Whoa!! Congratulations Sara, Natalia, and the rest of the team, great work!!

Today we are publishing 2 MANUSCRIPTS in @NatureComms 1. @NataliaPardoL discovers the role of nuclear MTHFD2 in centromere stability 2. Espinar and Garcia-Cao reveal the role of nuclear IMPDH2 in the DNA damage response. Nuclear Metabolism is on 🔥

🔬 FEBS Open Bio Webinar: Mitochondrial Biogenesis: An in-depth look into the beating heart of the eukaryotic cell 🗓️19th November at 16:00 CET ➡️zoom.us/webinar/regist… ➡️ network.febs.org/posts/upcoming… #mitochondria #webinar #FEBSOpenBio #YoungFEBS #FEBS_JS #febsjuniorsection

Last week's papers on #glutamine #cancer and #metabolism via @Bims_BiomedNews biomed.news/bims-glucam/20… Top pick: Glutamine modulates neutrophil recruitment and effector functions during sterile inflammation pubmed.ncbi.nlm.nih.gov/39504570/

ICYMI. The #hallmarks of #cancer #immunoevasion. After the 3 Es, the #3Cs, a new framework from @ClaudiaGalassi9 @IlioVitale @GeneCollector and co. On the cover of @cancer_cell Beatiful design by Cris Iribarren offtwitter. Available at cell.com/cancer-cell/fu… @FoxChaseCancer

@RyanLab_MBU @MRC_MBU excellent news Dylan, well deserved!

Quiet a nice moment in my early academic career to be nominated for a research culture award 😃 @MRC_MBU

📢Last two weeks of #immunometabolism discoveries @Bims_BiomedNews ⬇️⬇️⬇️ biomed.news/bims-imicid/20… biomed.news/bims-imicid/20…

Out today @NatureAging ! Life stress can accelerate aging and shorten lifespan, but how remains unclear. We identify that hippocampal/cortical neurons acquire features of p16-dependent #senescence and DNA damage in mice exposed to chronic social stress. nature.com/articles/s4358…