Sorry. I can’t provide medical advice here. I recommend talking to your doctors

I don’t think so. This appears to be unique to dermatomyositis

Maybe we should have done this in the early days of Covid

3/n
They are so prevalent in our genomes (>1 million copies) and because of their sequence similarity, they anneal to each other creating dsRNA capable of triggering innate sensors leading to interferon production. My work showed a big increase in expression of these Alus in dermatomyositis muscles

2/n
But you know what looks like a virus: Alus! a type of non-coding RNA that has been copy-pasting itself in our genomes (they've done this so much that our genome is 10% Alus)

Fascinating! This will be a fun story to tell at dinner parties

Thank you

A great read, thank you

I study genomics in autoimmunity. As an outsider to the field, I appreciated your introduction discussing mediocre efficacy of drugs targeting plaques. Do you expect this indirect way of targeting plaques to have better efficacy? or do microglia have other effects that are independent from plaques?

2/2
- What if new peptides not seen before by the immune system are made in lupus through dysregulated splicing? Can these become neoantigens driving autoimmune responses?

I’ll remember this the next time I order toci!

Interesting take. I appreciate highlighting the role of cytokines in infection pathology. I think what we currently call interferonopathy will still be different because the interferon abnormality is sufficient to cause disease.