Our paper is (finally) out in @CellRepMed: antibodies from #LongCOVID patients transfer symptoms to mice, pointing to a potential causal role for autoimmunity: @amsterdamumc @UMCUtrecht 1/12 cell.com/cell-reports-m… Long COVID has long been linked to autoimmunity.

But a key question remained:
👉 Are these antibodies causing disease, or just a byproduct?

We set out to test this directly. 2/12

Long COVID patients show immunological imprinting and impaired antibody class switching: fewer IgG/IgA antibodies against SARS-CoV-2 spike, but more against seasonal coronaviruses.
Interesting finding by my PhD student Ashwin Mak in J Med Virol: 1/6onlinelibrary.wiley.com/doi/10.1002/jm… Aberrant immune responses have long been suspected to play a role in #LongCOVID.
Here, we examined antibody profiles against both SARS-CoV-2 and the “everyday” seasonal coronaviruses. 2/6

For people that suffer from post-COVID-19 dizziness (as their ONLY symptom), this case report may be of interest to you: . A tale from personal experience… 1/10casereports.bmj.com/content/18/6/e… Disclaimer: we think that cases like this are rare. Yet, if you do suffer from this, the good news is that the cause of dizziness could be easily fixed by an ear nose and throat doctor (and some specialized vestibular physiotherapy). 2/10

I’m really impressed by the high level of research that was presented at the International ME/CFS Conference 2025 #mecfsconference, organized by the great @C_Scheibenbogen: . I’ll mention a few (personal) highlights: 1/7 events.mecfs-research.org/en/events/conf… First of all, this quote from @C_Scheibenbogen: “The most expensive thing we can do is not fund biomedical research and trials." Nothing to add there... 2/7

Last summer several interesting papers came out on #longcovid. I’ll mention a few that I found were particularly interesting. 1/7 I have to start with the great review about Long COVID science, research and policy in @NatureMedicine. The breadth of this review (including the economic burden) is unparalleled: 2/7nature.com/articles/s4159…

A strong indication for #autoimmunity in #longcovid: transfer of antibodies of patients induces symptoms in mice. Check out our latest preprint @biorxivpreprint: 1/11biorxiv.org/content/10.110… Before we start, beware that this is a preprint, and still needs to undergo peer review. Yet, since we believe these findings could be (very) relevant, let’s already have a look at what we found. 2/11

Several people asked me for highlights of the #longcovid Keystone conference #KSLongCoVID24. I’ll mention a few, personal, highlights. 1/x #KSLongCoVID24 highlight #1. First, the fact that we finally have a dedicated #longcovid meeting! Really feels like this research field has finally started, with scientists meeting each other for the 1st time. Let’s hope many meetings will follow (@KeystoneSymp 😉) 2/x

We previously showed that IgG antibodies strongly promote inflammation in severe COVID-19. But what about IgG induced by mRNA vaccines? Fortunately, no pathogenic IgG response there: biorxiv.org/content/10.110…. A thread. 1/7 In severe COVID-19, IgG induces inflammation because of two things: (1) different glycosylation of the antibody’s Fc tail (low fucose, high galactose) (2) enormous amounts of this IgG. Upon mRNA vaccination, these both happen, BUT: not simultaneously. 2/7

Why do #COVID19 patients become critically ill after around 1.5 weeks? Our @ScienceTM publication provides an explanation (and potential therapy). See our movie+article+thread for why we think this could be (very) important: 1/14 Super-short summary: We found (1) Why we become so sick (-> aberrant antibodies against Spike) (2) A drug that can counteract this (-> fostamatinib). Paper: stm.sciencemag.org/lookup/doi/10.… Now let’s go for some more detail. 2/14

Aberrant #glycosylation of anti-Spike antibodies promotes #thrombosis as observed in severely ill #COVID19 patients. Very interesting work from our collaborators in the UK: biorxiv.org/content/10.110…. A few thoughts on why this could be important. 1/4 Severely ill patients make IgG with aberrant glycosylation. We previously showed that this (over)activates lung macrophages, which in turn activates endothelium, which in turn activates platelets. But this paper shows that the antibodies (over)activate platelets directly! 2/4

IgG subclasses (IgG1/2/3/4) promote pathogen-specific immunity: jimmunol.org/content/early/…. Congratulations @WillianneHoepel @sona_all on this great work @J_Immunol. A small thread to summarize these findings and their potential implications 1/6 IgG antibodies come in 4 different flavors, known as subclasses: IgG1/2/3/4. According to the current paradigm, IgG3 is the most inflammatory subclass, while IgG2 and IgG4 are sometimes even considered to be anti-inflammatory. But that paradigm now seems to be outdated. 2/6

Why do #COVID19 patients often become critically ill around 1.5 weeks? Our latest work (now on @biorxivpreprint) may provide an explanation (and therapy) for this: aberrant IgG antibodies. A thread on why we think this could be (very) important: biorxiv.org/content/10.110… 1/7 First, we identified that anti-Spike IgG from serum of severely ill COVID-19 patients induces a hyper-inflammatory response by lung macrophages. This closely resembles the previously described ‘cytokine storm’ observed in COVID-19 patients. Yet, it does more. 2/7