Ahmad Yatim

Saidoune, Gilliet , @ahmad-yatim.bsky.social et al. show that excessive TLR7 responses to #SARSCoV2 by pDCs are linked to I-IFN–driven chilblain development. rupress.org/jem/article/...

From our Pattern Recognition Receptors & Beyond #InnateImmunity collection: rupress.org/jem/collecti...

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1/ I was honored to accept the 2025 Novo Nordisk Prize from @novo-nordisk.bsky.social at today’s award ceremony in Copenhagen, Denmark. It was a wonderful day that included a tour of The BioInnovation Institute, lunch at @novo-nordisk.bsky.social, and an evening award celebration and dinner.

Enhanced TLR7-dependent production of type I interferon by pDCs underlies pandemic chilblains, say Fanny Saidoune, Michel Gilliet, Ahmad Yatim (@ahmad-yatim.bsky.social) @casanovalab.bsky.social and colleagues: rupress.org/jem/article/...

#SARSCoV2 #COVID19

#WeekendRead! #MysterySolved! Saidoube @casanovalab.bsky.social Gillet @ahmad-yatim.bsky.social &co show @jem.org that excessive TLR7 activation in pDCs drives type I #Interferons protecting against SARS-CoV-2 but at the same time causing chilblains!
rupress.org/jem/article/...

18/ Thanks to Fanny Saidoune and all co-authors @jeremie-le-pen.bsky.social, @shenyingzhang1.bsky.social , @darraghduffy.bsky.social

17/ Huge thanks to the teams, particularly Michel Gilliet and @casanovalab.bsky.social Thanks to CHUVLausanne, @rockefelleruniv.bsky.social , ThrasherFund, EADV, and @institutimagine.bsky.social

COVID HUMAN GENETIC EFFORT COVID Human Genetic Effort is an international consortium aiming to discover inborn errors of immunity underlying severe forms of COVID-19 in previously healthy individuals

16/ We are now investigating whether affected individuals carry monogenic variants that enhance TLR7-mediated immunity to SARS-CoV-2 or other ssRNA viruses through the enrollment of a dedicated cohort worldwide through the COVID Human Genetic Effort (www.covidhge.com)

15/ The next step involves the exploration of this phenotype from a genetic angle. The observation of multiple family members developing PC simultaneously supports a genetic predisposition with a dominant inheritance pattern

14/ This observation also suggests that other forms of primary chilblains (“seasonal” chilblains) may be induced by similar phenomena triggered by winter-specific ssRNA viruses

13/ The study offers a mechanistic explanation for both the increased incidence of primary chilblains during the pandemic and the absence of conventional markers of adaptive responses in affected individuals

12/ The strong I-IFN activity in individuals with PC, particularly via TLR7 and by their pDCs, may have conferred a sterilizing innate immunity to SARS-CoV-2, limiting antigen availability for adaptive priming

11/ Chilblain lesions subsequently result from the infiltration of activated pDCs in acral skin, with I-IFN-mediated inflammation

10/ Patients’ pDCs exhibited cell-intrinsic hyperresponsiveness to TLR7 stimulation, but not TLR9, at odds with TLR7-deficient patients who are prone to life-threatening COVID-19 pneumonia

9/ We found that patients' leukocytes produced abnormally high levels of I-IFN when stimulated with ssRNA viruses, especially SARS-CoV-2, but not DNA viruses

8/ We hypothesized that individuals with PC are predisposed to the mounting of enhanced I-IFN responses to SARS-CoV-2, promoting early viral clearance and manifesting clinically as chilblains

Type I interferon response and vascular alteration in chilblain‐like lesions during the COVID‐19 outbreak* SummaryBackground. The outbreak of chilblain‐like lesions (CLL) during the COVID‐19 pandemic has been reported extensively, potentially related to SARS‐CoV

7/ While some authors attributed PC outbreaks to behavioral changes during lockdown, accumulating evidence supports an innate immune phenomenon triggered by the virus

academic.oup.com/bjd/article/...

jamanetwork.com/journals/jam...

6/ The temporal clustering of PC and COVID-19 cases suggests a causal link. However, most patients tested negative for SARS-CoV-2 by PCR and failed to mount detectable adaptive responses (overall IgG seroconversion <10%)

Are ‘COVID toes’ actually caused by the coronavirus? Study adds to evidence suggesting that SARS-CoV-2 infection doesn’t cause an inflamed-toe condition called chilblains, but it doesn’t close the door.

5/ During the COVID-19 pandemic, the surge in chilblain cases among otherwise healthy individuals, often described as “COVID-toes” or pandemic chilblains (PC), garnered widespread scientific and public interest

www.nature.com/articles/d41...

4/ Before the pandemic, primary chilblains were rare, typically occurring in the winter and coinciding with the circulation of seasonal ssRNA viruses, such as common coronaviruses, RSV, and influenza. However, no direct link to viral triggers had been established before 2020

3/ Chilblains can occur secondary to chronic type I interferon (I-IFN)-driven conditions such as monogenic interferonopathies and #lupus, or primary, when striking otherwise healthy individuals

2/ Chilblains are inflammatory papules that appear on acral sites. First described in 1888, they have remained a medical mystery for more than a century

1/ One of the most intriguing enigmas of the #COVID19 pandemic was the sudden and unprecedented outbreak of chilblains that accompanied the early waves of #SARSCoV2 infections. Our new study in @jem.org uncovers the underlying immunological mechanism

rupress.org/jem/article/...

Enhanced TLR7-dependent production of type I interferon by pDCs underlies pandemic chilblains @jem.org @casanovalab.bsky.social rupress.org/jem/article/...

Chilblains were reported in #SARSCoV2–exposed individuals without PCR- or serologically defined #COVID19. Saidoune, Gilliet , @ahmad-yatim.bsky.social et al. show that excessive TLR7 responses to SARS-CoV-2 by pDCs are linked to I-IFN–driven chilblain development. rupress.org/jem/article/...

1/ I am both delighted and relieved to share my inaugural editorial for the @jhumimmunity.org
rupress.org/jhi/article/...

Excited to launch this new journal with a great team, and the support of both RUP and IAPIDS, and the entire community of human inborn errors of immunity !

What Happens When Some Cells Are More Dad Than Mom (and Vice Versa)? A new study shows that some of our cells favor genes of one parent or the other and can explain a longstanding mystery of why some people with disease-causing genes experience no symptoms.

What Happens When Some Cells Are More Dad Than Mom (and Vice Versa)?
Latest from us. Published today. News here www.cuimc.columbia.edu/news/what-ha... article here: www.nature.com/articles/s41... @stewart_ojay @BogunovicLab and a huge international team thank you 🙏🏼