[conspire] Auto Immune

Deirdre Saoirse Moen deirdre at deirdre.net
Tue Apr 14 21:23:07 PDT 2020


On Tue, Apr 14, 2020, at 5:37 PM, Texx wrote:
> I only know a little about auto immune issues, but I believe we have at least one person on this list dealing with it.
> 
> Are cytokines part of the problem in auto immune disease (Lupus, Rheumatoid Arthritus etc) ?

Oooh, I've learned a lot on this in the last couple weeks.

First, a fascinating tidbit: one of the reasons women suffer more from autoimmune issues is the X chromosome is longer than the Y chromosome. So, having two copies, women get more immune signalling capability, as that's mostly what's encoded in that length difference. That has its advantages and disadvantages.

Second, it means women (of the XX sort) tend to live longer, on average (globally), even when you take maternal mortality into consideration, because disease fighting capability. Note that even though women have higher BMIs generally and are more likely to be obese *and* obesity's been a stated factor for winding up in the hospital/ICU/dying of COVID-19, the numbers consistently show that's not happening. [1]

Now, onto your question: Yes and no. They're a signaling molecule, and when you hear antibody, for example, that is ONE type of cytokine.

So basically part of the function of your immune system is to keep your various parts where they're expected to be, and that's complicated. Self/non-self recognition is incredibly complex and imperfect and is intended to keep your organs and muscles and stuff intact, but also keep cancers from spreading. Unfortunately, this also means that things can be mis-recognized if they appear too similar, which is what celiac disease is. (Oh? Gluten attached to an intestinal cell? Let's destroy that fucker! Seriously.)

The cytokine storm that is killing COVID-19 patients is interesting, and I've been reading up on it and it's…horrifying. It is actually more dengue-like than I thought at first, I just didn't have the words to do the search. 

So in antibody-dependent enhancement a la dengue, having antibodies to one form helps the immune system say, "Ah, I know this, let's make some cytokines!"

Except it just keeps going and going and going like the everready bunny. In dengue, this can cause a hemorrhagic form if you catch it a second (or later) time.

https://www.statnews.com/2017/11/02/dengue-second-infection/

Well, it turns out that that is actually more common than we thought, it's just that it's more obvious in dengue infections than in other viruses.

So it turns out that the problem with creating vaccines, and the problem with injecting convalescent plasma, etc., is figuring out the right load to *not* create a cytokine storm. Because you want to kick the immune system, you just don't want to drop kick it.

And therein lies the rub.

See comments here: https://www.reddit.com/r/COVID19/comments/fzvbgs/the_sarscov2_receptorbinding_domain_elicits_a/

Deirdre


[1] Except Kansas, which is weirdly, the only jurisdiction globally I've seen with flipped statistics. But, you know, Kansas. https://public.tableau.com/profile/kdhe.epidemiology#!/vizhome/COVID-19Data_15851817634470/KSCOVID-19CaseData
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