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You and me both :) I was able to find some potential connections between NLRP3 and lipid metabolism through the transcription factor SREBP (which controls lipid-related genes in a lot of cells and would be one of the more downstream switches in B cells)...

Ah okay, thanks for clarifying. I think a lot of the pushback comes from myself and several others on the thread interpreting the comment below and others from your posts as you arguing against a unifying mechanism. [Edit: I think everyone here is on board with the idea that rare variants could...

Good point.

maybe! I think when the questions become “is it possible that X part of the immune system could have an impact on Y part of the immune system?” the answer will pretty much always be yes—you just need specific observations to determine whether that interaction has enough strength to really...

Here’s the paper I was thinking of from Bali Pulendran’s lab about lipid regulation in B cells: https://pmc.ncbi.nlm.nih.gov/articles/PMC10928801 It identified the transcription factor SREBP as the “master regulator” of B cell lipid metabolism—though other transcription factors could (and...

I am not sure! I assume that NLRP3 related processes happen somewhat independently from B cell responses, though there may be points where they overlap and interact

Yup I think we might be at an impasse. I’m all for pulling pieces of information into a hypothesis, but the concern is that an analysis like this is structured to introduce multiple layers of confirmation bias where a different kind of analysis wouldn’t—from the way specific genes are picked out...

Found one of the papers I was thinking of: https://www.nature.com/articles/s12276-022-00729-9 I landed on it while following up on my interest in mtDNA/interferon, but viral DNA activates the same sensor. Though selfishly I’m now wondering if a ZNFX1 mutation could be relevant in both...

Yeah, potentially. I think many biology grad students will be completely upfront that the reason they keep producing the same somewhat ugly jitter plots is just because they have zero coding knowledge, know how to use one plotting software with a UI, and that's the type of plot it produces...

Yup violin plots are definitely used for that reason--though often jitter plots convey sample density better than a violin because violins get scaled to the width of their "lane" on the x axis. If it was important to convey that one group had way more samples than another I might opt for jitter...

Yeah that's a potential way to look at it--virus would be detected by and induce different facets of the immune response simultaneously (through intracellular RNA/DNA sensors, TLRs, inflammasome, adaptive recognition, etc.), each of which trigger different combinations and strengths of...

Sure, I tend to use violins often. I'm not sure if the right hand side dots are the best way to convey information about density though

So I guess my concern is that I don't see that level of strong evidence for most of the variants pulled out in this study. The evidence is those handful of case studies but the conclusion is that the relevance of the results is akin to something with strong evidence [edit: and even in this...

I see your point here, but I think the key difference re: this paper is the difference between pointing to a rare variant as a potential causal factor predisposing to falling into a chronic disease feedback loop and pointing to a rare variant to claim that the person actually has a rare genetic...

So my main point is still a concern here: that n-of-1 approaches will always end up quite biased towards overestimating the relevance of specific variants for symptoms that might be better explained otherwise. It bears asking what "well-supported" late-onset symptoms of a heterozygous variant...

It’s one part of myeloid pathogen recognition, leading to caspase and IL-1B induction plus some other cytokines I’m forgetting (though I don’t think interferon is one of the main ones)

Thanks for the back and forth @LizWorthey

It’s something that is necessary in research by virtue of not knowing the mechanism of ME/CFS and not having any objective measure to test for. It is entirely possible that someone could end up with the entity known as ME/CFS by multiple mechanisms. That being said, if someone has a genetic...

I also don’t think we can discount the possibility that the glymphatic channels might have just been unintended byproducts of evolving a system which added extra checkpoints and barriers between the brain parenchyma and the circulation to keep the extracellular space around neurons relatively...

My bad, I thought you were asking “and why” there were missing values