Mashreghi_Lab

Our latest study in @nature reveals how #TGFβ drives Epstein-Barr Virus (#EBV) reactivation in multisystem inflammatory syndrome in #children (#MISC, #PIMS) following #COVID19. @DRFZ_Berlin @Mashreghi_Lab #SARSCoV2 @ChariteBerlin 🔗 Read here: nature.com/articles/s4158…

@Moooonflash @JackHadfield14 @amaticahealth Here, we uncover the role of TGFβ in MIS-C—the first recognized post-COVID-19 syndrome in children. But also in severe COVID-19. nature.com/articles/s4158…

@JackHadfield14 @amaticahealth "SARS-CoV-2 in severe COVID-19 induces a TGF-β-dominated chronic immune response that does not target itself" nature.com/articles/s4146…

In Long Covid & ME/CFS @amaticahealth identified statistically increased free/active serum TGF-β1, but normal total TGF-β1 Which shows the nuance in testing. Will have more data soon from an additional 60 LC & ME individuals.

Nice to see our @Nature paper (rdcu.be/e4o4z) validated again, even without a citation. Prolonged TGF-β locks NK cells in dysfunction. biorxiv.org/content/10.648…

Scientific memory can be surprisingly short. 📚❓🧠🕳️

Confirmation is welcome: TGF-β–driven pathology in severe COVID-19 and post/longCOVID;rdcu.be/e2vBi; rdcu.be/e2vFn; were described by us in 2021 rdcu.be/e2vHo and in a defining post-COVID disease rdcu.be/e2vIL, (2025). Regrettably, uncited

Big kudos to the whole team for pulling together clinical trial execution, single-cell biology, and translational immunology so elegantly. Honored to have been part of this effort. @Mashreghi_Lab @ChariteBerlin German_Rheumatology Research Center; DRFZ @LeibnizWGL

This work strongly supports ASCs as central drivers of disease activity in SLE, and CD38 as a clinically actionable target—opening the door for smarter combination or sequential therapies.

New paper out in Nature Communications Huge congrats to Lennard Ostendorf and Tobias Alexander on a really impressive phase 2 trial in SLE. Very happy to have contributed to this work. #citeas" target="_blank" rel="nofollow noopener">nature.com/articles/s4146…

KI hilft am Deutschen Rheuma-Forschungszentrum Rheuma zu entschlüsseln. Wie funktioniert das? Julia Bidder sprach dazu mit PD Dr. Mir-Farzin Mashreghi vom DRFZ und Dr. Vikram Sunkara vom Zuse-Institut Berlin (ZIB). rheuma-liga.de/unser-einsatz/…

Shared TCR Vβ21.3+ T cell immunological signature between MIS-A and MIS-C rupress.org/jhi/article/2/…

@GertrudRey In MIS-C, EBV is easier to detect as a driver of hyperinflammation because many children are EBV-negative at baseline, unlike adults. nature.com/articles/s4158…

However, because most adults have antibodies against EBV and there was no significant difference in the percentage of EBV antibody-positive participants between experimental and control groups, it is unlikely that a positive EBV antibody status contributes... 18/

Why do some people develop long COVID while others do not? While we still don't know for sure, some answers are beginning to emerge. In this 🧵 I describe some groundbreaking work done by @VirusesImmunity at Yale in an attempt to answer this question. 1/

@ZdenekVrozina Strong data for lupus. However, in MIS-C, EBNA2-specific T cells are hyperactivated yet fail to control EBV, driving inflammation. Same virus—distinct immune failure modes across diseases. nature.com/articles/s4158…

And it probably won’t stop there. The same EBV B-cell circuit, EBNA2 rewiring, chronic T-cell activation - shows up in other autoimmune diseases too - MS, rheumatoid arthritis, even Crohn’s. One virus, many faces? Breakthrough study.

A new study may finally explain how EBV triggers and worsen lupus. A paper in Science Translational Medicine + Stanford Medicine report just clarified a question researchers have chased for decades.
How can a virus that almost everyone carries ignite lupus in some people?🧵

Mashreghi Lab Christmas dinner 🎄✨ Great food, great people, great science — the perfect way to close the year together. Looking forward to new projects and breakthroughs in 2026! #TeamScience

@VirusesImmunity Absolutely. This is especially relevant for children with post-COVID syndromes including MIS-C, where EBV reactivation and impaired antiviral immunity play a major role. Our recent Nature paper provides direct evidence for this link: nature.com/articles/s4158…

EBV is implicated in other autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, Sjögren’s syndrome, as well as post-acute infection syndromes (Long COVID, ME/CFS) and malignancies. Vaccines and antivirals to block EBV are urgently needed. (end)

A groundbreaking paper by @younis_sh1 et al. @stanfordimmuno provides an answer to the long-standing question about how EBV infections are linked to lupus. A short thread to explain the key findings. (1/) science.org/doi/10.1126/sc…

New paper on TGFβ and TNF in post-COVID syndrome great to see growing recognition of TGFβ pathway we previously described in long-term immune dysregulation following COVID-19. rdcu.be/ePG6V, rdcu.be/ePG7f, rdcu.be/ePG7U, rdcu.be/ePG8t