Vijay Rathinam
@vijayrathinam.bsky.social
1K followers 230 following 45 posts
Professor of Immunology, UConn Health School of Medicine. Studying innate immunity, infection and inflammation. https://facultydirectory.uchc.edu/profile?profileId=Rathinam-Vijay2
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vijayrathinam.bsky.social
Why does RNA undergo glycosylation? Excited to have our paper out. We in collab w/ Ryan Flynn @raflynn5.bsky.social show N-glycans on glycoRNA hide self-RNA from endosomal TLRs promoting silent removal of dead cells. www.nature.com/articles/s41... @uconnresearch.bsky.social @uconnhealth.bsky.social
Reposted by Vijay Rathinam
raflynn5.bsky.social
We’re excited to report work led by postdoc Jennifer Porat in the lab, finding that DNA accumulates on the surface of living cells and that the secreted extracellular protein DNASE1L3 can modulate its levels on B and T cells. With a new twist for ATAC-seq as well www.biorxiv.org/content/10.1...
DNASE1L3 surveils mitochondrial DNA on the surface of distinct mammalian cells
The extracellular space is a critical environment for discriminating self versus non-self nucleic acids and initiating the appropriate immune responses through signaling cascades to relay information ...
www.biorxiv.org
Reposted by Vijay Rathinam
avishenoy.bsky.social
📢A new effector-triggered immunity role for GBP1! No place for pathogens to hide now that GBP1 can detect extracellular pathogens that hijack the actin cytoskeleton. Surprise*suprise* GBP1 does this independently of LPS! 🧵
biorxiv.org/content/10.1...
Reposted by Vijay Rathinam
nizet.bsky.social
Pleased to share and briefly highlight our new manuscript just published 𝘑𝘊𝘐 𝘐𝘯𝘴𝘪𝘨𝘩𝘵 (a short🧵)

"A STING-adjuvanted outer membrane vesicle nanoparticle vaccine protects against lethal 𝘗𝘴𝘦𝘶𝘥𝘰𝘮𝘰𝘯𝘢𝘴 𝘢𝘦𝘳𝘶𝘨𝘪𝘯𝘰𝘴𝘢 pneumonia"

🔗 doi.org/10.1172/jci....
Reposted by Vijay Rathinam
Reposted by Vijay Rathinam
colllab.bsky.social
So excited that this study is now online! It's been a pleasure to work with BioAge Labs and our collaborators on this story. We characterise a new class of #NLRP3 inhibitors with translational potential for so many inflammatory diseases.
jem.org
#NLRP3 is a target for antiinflammatory therapies & can be inhibited by the tool compound MCC950. Wilhelmsen, @colllab.bsky.social et al characterize new small-molecule inhibitors, BAL-0028 & BAL-0598, that have a distinct mechanism of action & binding site. rupress.org/jem/article/...
#Inflammasome
Reposted by Vijay Rathinam
lozanzi.bsky.social
#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...
vijayrathinam.bsky.social
Congratulations Ryan! Well deserved!!
vijayrathinam.bsky.social
Thanks Ivan for sharing!
vijayrathinam.bsky.social
Thanks Steve for sharing!
Reposted by Vijay Rathinam
labwaggoner.bsky.social
@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...
Reposted by Vijay Rathinam
madison-strine.bsky.social
Check out this @nature.com paper from the brilliant scientist I get to call my husband!!!!
vinnieviruses.bsky.social
Hi everybody! I am super excited to share the work done during my PhD published in @nature today! We describe a new mechanism of self- vs. non-self RNA discrimination by showing how N-glycans shield glycoRNAs from stimulating endosomal RNA sensors www.nature.com/articles/s41...
RNA N-glycosylation enables immune evasion and homeostatic efferocytosis - Nature
N-glycans on glycoRNAs prevent innate immune sensing of endogenous small RNAs, and the natural mechanism they use demonstrates how glycoRNAs exist on the cell surface and in the endosomal network with...
www.nature.com
Reposted by Vijay Rathinam
raflynn5.bsky.social
The work brought together a lot of expertise from labs including Penghua Wang, Michael R. Wilson, Sivapriya Kailasan Vanaja, Beiyan Zhou, Franck J. Barrat, and Thomas Carell - and we were critically supported by grants from NIH (NIGMS, NIAID, NIDDK) and scleroderma research foundation
Reposted by Vijay Rathinam
raflynn5.bsky.social
Finally, we found that the de-N-glycosylated RNA is sensed through both TLR3 and TLR7 which could suggest that encoding both ssRNA and dsRNA motifs with acp3U and thus dual engagement of TLR3 and TLR7 provide sufficient signal threshold.
Reposted by Vijay Rathinam
raflynn5.bsky.social
We defined the chemical moiety causing this stimulation to be the core RNA modification of acp3U, which we had previously found to be a covalent linker between RNA and N-glycans (Xie et al. Cell 2024). We confirmed this with chemical synthesis RNAs containing only 1 acp3U.
Reposted by Vijay Rathinam
raflynn5.bsky.social
This effect was also true on the surface of apoptotic material which is normally cleared via efferocytosis in an immune silent process. Loss of N-glycans on this material triggers innate immune cells.
Reposted by Vijay Rathinam
raflynn5.bsky.social
We found that de-N-glycosylation of purified small RNA using PNGaseF causes the RNA to be immunostimulatory to both mouse and human macrophages
Reposted by Vijay Rathinam
raflynn5.bsky.social
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...