Posts by Vincent Graziano
I'm glad to see this being covered - because, frankly, this is a death-blow to collaborative science - however, the assumption of good faith in any of these decisions by reporters is mind-boggling.
This is happening for one reason - to assure top-down control of what gets funded and what does not.
Out today in Nature - our collaborative work with Ryan Flynn's lab, led by Dr. Peiyuan Chai with support from Dr. @sinakheiri.bsky.social and @shahjess.bsky.social from our group. Exciting findings showcasing how glycoRNAs can modulate angiogenesis!
Huge advance in glycoRNA biology. Congrats to @raflynn5.bsky.social and all of the wonderful authors! Can’t wait to see what you guys do next!
Thanks to Autoimmunity podcast @kevinbonham.bsky.social & @woodrufflab.bsky.social for discussing our glycoRNA paper w/ @raflynn5.bsky.social @vinnieviruses.bsky.social
Thank you for covering our paper!
In our latest episode, @woodrufflab.bsky.social and @kevinbonham.com talk about glycoRNAs, and the way they're shielded from the immune system in a new paper from the labs of @raflynn5.bsky.social and @vijayrathinam.bsky.social 🧪
audiommunity.org/episodes/epi...
Sugar coats shield immunogenic RNA modification:A new function for RNA glycosylation: Molecular Cell www.cell.com/molecular-ce... @raflynn5.bsky.social @vinnieviruses.bsky.social
Don’t trust the experts”? That’s not democracy, that’s recklessness.
On a plane, I want a pilot.
In a hospital, I want doctors and scientists who understand the evidence.
Expertise isn’t religion or authoritarianism — it’s training, accountability, and data.
Ignore it and we all pay the price.
🚨New Paper in Cell 🧵🔎
Happy to share our work led by the @camilahcoelho.bsky.social, on mAbs against mpox.
We were very excited (and lucky!) to contribute to this collab. effort.
🦠“Human monoclonal antibodies targeting A35 protect from death caused by mpox”🦠
doi.org/10.1016/j.cell.2025.08.004
#InterferonPower! Thrilled for our latest work @cp-cell.bsky.social! With @danielboehmer.bsky.social, we dug into tons of papers & created what we hope will be a go-to resource for immunologists & non-immunologist about type I, II, III (& IV😉) #interferons! Free👉 authors.elsevier.com/a/1leKGL7PXu...
Another piece of the #glycoRNA puzzle revealed by @raflynn5.bsky.social and @vijayrathinam.bsky.social!! RNAs with modified base acp3U activate TLR3/7, but not when acp3U is N-glycosylated. This is how cell surface/secreted glycoRNAs avoid stimulating autoimmunity.
www.nature.com/articles/s41...
4/5 The Glycobiology Significant Achievement Award:
Dr. Ryan Flynn @raflynn5.bsky.social, Harvard University, 👏👏🥂
Thanks Dr. Doench! Hope you’re doing well!
@vijayrathinam.bsky.social @vinnieviruses.bsky.social @raflynn5.bsky.social discovers why RNA undergoes glycosylation: N-glycans on glycoRNAs hide self-RNA from endosomal TLRs promoting ‘silent’ clearance of dead cells @nature.com
www.nature.com/articles/s41...
Incredible discovery ! The first known role for sugar coated RNAs : immune evasion ! @raflynn5.bsky.social does it angain with @vinnieviruses.bsky.social @vijayrathinam.bsky.social and colleagues !
Check out this @nature.com paper from the brilliant scientist I get to call my husband!!!!
RNA N-glycosylation enables immune evasion and homeostatic efferocytosis by chemically caging acp3U. Excited to report this work lead by Vinnie @vinnieviruses.bsky.social and in collaboration with @vijayrathinam.bsky.social in @nature.com www.nature.com/articles/s41...
Big congrats to Vinnie Graziano @vinnieviruses.bsky.social who led the project and huge thanks to our great collaborators: Jennifer Porat, Thomas Carell, Franck Barrat, Beiyan Zhou, Sivapriya Kailasan Vanaja, Michael Wilson, and Penghua Wang!! #innate_immunity #interferon #celldeath
Together, these data reveal one of potentially many answers to the question “why are RNAs glycosylated?” to which we found that it is to prevent autoinduction of RNA-sensing pathways.
Lastly, we found both TLR3 and TLR7 are required for sensing acp3U containing RNAs.
We teamed up with the Carell lab who synthesized an 18-nt long native or acp3U-containing RNA and found acp3U-RNAs were more immunostimulatory than the unmodified RNAs.
To our surprise, cells deficient in acp3U were not able to stimulate macrophages in both our transfection and efferocytosis assays.
Recently, it was found that acp3U (a hypermodified uridine) is an attachment site for N-glycans to RNA. Genetic KOs of the enzyme DTWD2 prevents the synthesis of acp3U resulting in decreased glycoRNA signal.
Injecting WT mice with deglycosylated apoptotic cells was also capable of inducing a localized RNA-driven innate immune response.
We found that treatment of apoptotic cells with PNGase F elicited a potent IFN response when fed to macrophages.
With this in mind, we asked if N-glycans on RNAs promotes the immunologically silent clearance of apoptotic debris through the process of efferocytosis.
Because glycoRNAs are predominantly on the cell surface, we asked how they would behave during apoptosis. For instance, apoptotic cells are cleared constitutively from our system without inducing inflammatory responses through the process of efferocytosis.
Next, we checked to make sure PNGase F was not acting on the cells to induce an IFN response. We treated long RNA fractions (containing no glycoRNAs) with or without PNGase F and observed no production of IFNb, confirming this requires deglycosylation of small RNAs.
Here, we harvested small RNA fractions (enriched for glycoRNA) and treated small RNAs with the N-glycosidase PNGase F. We found that removal of the N-glycan renders these RNAs immunogenic upon transfection. Addition of RNases was able to abrogate this response.