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#autoimmunity

0 posts0 participants0 posts today
Sibylle Dahrendorf

🎥 #Documentary #ChronicallyIgnored

Only a few days left until June 20th. I would be very grateful for sharing, so that as many people as possible can be reached! Thank you so much for your support!

A Wake-Up Call To Politics, Medicine & Research

#POTS #SmallFiber #SIBO #Autoimmunity #MCAS #FQAD #FQToxicity #FlagylToxicity #EDS #hEDS #Marfan #CCI #LongCovid #LongLyme #VacInjury #LongList #LongTragedy

Film Link here:
🎥vimeo.com/ondemand/chronically

datum (n=1)

Ok, so remember the whole "COVID-19 seems to have superantigenic properties but it's not clear which of its proteins drive that" thing?

Persistent N protein in peripheral blood might be one driver of autoimmunity: disabled.social/@tomkindlon/11

Preprint: BioRxiv The Role of SARS-CoV-2 Nucleocapsid Protein Persistence in Inducing Chronic Type I Interferon and Mitochondrial Dysfunction — Andreas Koenig et al. "our findings suggest that the persistence of SARS-CoV-2 N-protein in peripheral blood promotes a chronic inflammatory milieu, even several months after active infection via MAVS-mediated type I IFN production that could contribute, in susceptible individuals, to the development of autoimmunity."
disabled.socialTom Kindlon (@tomkindlon@disabled.social)Attached: 1 image US research: "our findings suggest that the persistence of #SARSCoV2 N-protein in peripheral blood promotes a chronic inflammatory milieu, even several months after active infection..." https://www.biorxiv.org/content/10.1101/2025.06.02.657400v1 Image from Science for ME update @longcovid@a.gup.pe #LongCovid #PASC #PwLC #postcovid #postcovid19 #Covidlonghaulers #PostCovidSyndrome #longhaulers #COVIDBrain #NeuroPASC @covid19@a.gup.pe #Coronavirus #COVID19 #COVID #COVID_19 #COVIDー19 @novid@chirp.social #novid @novid@a.gup.pe #CovidIsNotOver @auscovid19@a.gup.pe #auscovid19
#CovidIsNotOver#COVID19#COVID
Replied in thread
conscientious objector🇨🇭🪂

@antiaall3s

The issue with those stories are, those are anecdotally.

Maybe beside the mediation she is:
using asthma or blood pressure medications. Maybe statins. Maybe the vaccine as she didn’t wanted a re-infection, maybe she had luck - as #autoimmunity after infections is actually common and often resolves 🤷‍♂️

So her communication is shit. But she is doing #sport not #medicine.

The one writing then story without using its brain is the issue. The stubborn physicians are an issue.

Tom Kindlon

"Research finds potential “molecular mimics” behind #COVID -induced #autoimmune disease"

eurekalert.org/news-releases/1

“some of the human proteins the researchers identified as likely targets of COVID-induced #autoimmunity are only found in people with specific genetics”

Hashtags:
@longcovid
#LongCovid #PASC #PwLC #postcovid #postcovid19 #Covidlonghaulers #PostCovidSyndrome @covid19 #Coronavirus
#COVID19 #COVID_19 #COVIDー19 #SARSCoV2 @novid@chirp.social #novid @novid@a.gup.pe #CovidIsNotOver
@auscovid19 #auscovid19

Science Updates

"An aging thymus leads to a 'leaky' immune system," said senior study author John White, a Professor and Chair at McGill University. "This means the thymus becomes less effective at filtering out immune cells that could mistakenly attack healthy tissues, increasing the risk of autoimmune diseases like type 1 diabetes."

#health #medicine #science #research #biology #autoimmunity #immunology

labroots.com/trending/cell-and

LabrootsWhy Vitamin D Deficiency Can Raise Autoimmune Disease Risk | Cell And Molecular BiologyThe body can naturally produce vitamin D when skin is exposed to sunlight, but this process declines significantly in winter. | Cell And Molecular Biology
Thiago Carvalho

'To elucidate the in vivo function of neoself-antigens presented on MHC-II by decreased Ii expression, we analyzed the antigen specificity of clonally expanded autoreactive T cells in SLE patients as well as in drug-inducible Ii knockout (Ii-iKO) mice, which allowed us to delete the Ii from adult mice. We demonstrate that neoself-antigens presented on MHC-II upon decreases in Ii expression levels are recognized by CD4+ T cells as non-self-antigens and are the primary targets for autoreactive T cells clonally expanded in SLE patients. Furthermore, we suggested that EBV reactivation, which downregulates Ii expression, could be involved in the activation of neoself-reactive T cells.'
#Immunology #Autoimmunity
sciencedirect.com/science/arti

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