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Laawlly t1_ivdkzy8 wrote

Reply to comment by cristiano-potato in We know about viruses, bacteria and other microorganisms evolving to better infect other organisms. Consequently, diseases change too to some extent. Are there any examples of human bodies evolving to fight against these disease causing agents? by ha_ha_ha_ha_hah

NK cells also have a repitior of activating receptors that fit pathogen antigens, in addition to missing-self signals. These receptors are are hardwired into our genomes to recognize the pathogens that have infected us generation after generation. Like cytomegalovirus.

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cristiano-potato t1_ivdn6hv wrote

Does this apply to both CD56dim and CD56bright NK cells? My understanding is that CD56dim NK cells generally need antibodies to mark cells for them whereas CD56bright NK cells will kill cells without them being marked.

Do they recognize COVID? I’ve been wondering if the better outcomes for COVID cases in active people, even after adjusting for co-morbidities (meaning that the effect sizes aren’t simply due to physical activity preventing obesity or diabetes) could be due to the fact that studies have shown moderate exercise increases NK cell proliferation as well as I believe macrophages and other cells. One study called it “enhanced immunosurveillence”. So maybe exercise increases the proliferation of NK cells which helps as a front line defense against COVID? NK cells are abundant in mucosa right?

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Laawlly t1_ivgfruw wrote

The CD56 status of NK cells indicates the "maturity" of the cell. CD56bright NK are less effective killers but have the ability to become CD56dim when stimulated. CD56dim NK have a greater number of activating receptors on their surface, including CD16, which is the receptor that binds to antibodies. But antibody mediated killing is just one of many ways that an NK cell can target infected cells.

As far as I know, there's no evidence that the covid virus is directly recognized by NK cells. But when normal cells become infected by any virus, they start to put out distress signals that an NK cell can recognize, idenpendent of the pathogen.

I would be interested in seeing the study that found that exercise increases the proliferation of NK cells. In my experience, the portion of NK cells in an individual is fairly stable over time - it does vary widely from person to person (5-15% of white blood cells).

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cristiano-potato t1_ivgil3k wrote

Yeah I don’t see how NK cells would recognize Covid virons directly, I did mean recognizing the infection by way of recognizing infected cells that are stressed.

I will paste the study I found prior when I am able to find it again, when I’m off mobile. I did find this one: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4909049/

Which talks about the studies examining the effects of exercise on NK cells, some studies report conflicting results but it seems this is often due to exercise dose.

I also wonder about things that are fairly common and usually benign like SIgAD, or far more commonly partial IgA deficiency (PIgAD). I found one study that found a 4x odds ratio for severe Covid in SIgAD patients, but the CIs are massive, this doesn’t apply to PIgAD (generally defined as IgA levels below 2SD of the median but not below detection limits, for example if reference range bottoms out at 90mg/dL and you find 30, that’s not <5 but it’s low), and also you have the bias inherent in the fact that many SIgAD people are asymptomatic so a cohort of diagnosed SIgAD people is going to probably include mostly symptomatic cases since they’re more likely to be detected.

But PIgAD is far more common, obviously simple math dictates a low single digit or slightly below 1% rate. If this is associated wifi more severe Covid outcomes I’d wonder what can be done for those patients since IgA deficiencies can’t really be “treated” effectively and even a mucosal / nasal vaccine would not help much if their B cells are being arrested before maturing to the point of creating IgA antibodies

Thanks for the explanation w.r.t. CD56.. I wonder what the most crucial element in the naive host is? Innate immunity wise. IgA? Can that be created quickly even if you’re immune naive? Thinking about back in 2020 how some immune naive hosts still had mild course. Or is it just that their innate immune system reacted quickly? Given the high concentration and extensive proliferation of neutrophils, they’d probably be the first to come across the infection and sound alarm bells no?

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