Genetics: Chromosome 6 BTN2A2 and BTN3A3 (BTN2A1)

[hotblack]

I may be wrong about this but I am not sure that NK cells have 'memory' in the usual sense. The rather similar CD57+ CD8 killer T cells would do. But I may be out of date.

Thanks Jonathan this is all really useful. Over recent months I’ve been reading some papers about memory or memory like NK cells, which after exposure to cytokines can hang around for a long time with lower thresholds for activation.

I’m not sure if this ties in with the behaviour you mention, or is something different, but in reminds me of the fc gamma receptor behaviour in your paper, just in a different cell.

My conceptual understanding is fuzzy and my brain is not feeling particularly sharp atm so I’m struggling with the actual mechanisms and may be misinterpreting things. Maybe when I can get it together I’ll start a thread and see what others can make of it.

 

[Jonathan Edwards]

Thanks Jonathan this is all really useful. Over recent months I’ve been reading some papers about memory or memory like NK cells, which after exposure to cytokines can hang around for a long time with lower thresholds for activation.

That is something have not caught up with. It would not be surprising. These would not carry memory in the sense of remembering a specific antigen but could be remembering recent danger signals and remaining in a 'primed' state through an epigenetic modification.

And yes, this is very much the area jnmaciuch and I were discussing in terms of which cells were carrying 'immune memory' in ME/CFS - whether expanded T cell clones or macrophages with epigenetic modifications or indeed maybe NK populations. The BTN story seemed to feed in to that question.

What we have no data on so far is where such cells might be hiding. Cells in bloodstream may be a very unreliable guide or even a decoy. Maybe the old data on reduced NK function/numbers reflects a real shift in NK behaviour, but maybe the primed cells are hiding away and not circulating.

 

[Kitty]

maybe the primed cells are hiding away and not circulating.

Guess it might somewhere difficult to examine, but could also be in plain sight in a busy location—like gut?

 

[hotblack]

What we have no data on so far is where such cells might be hiding. Cells in bloodstream may be a very unreliable guide or even a decoy. Maybe the old data on reduced NK function/numbers reflects a real shift in NK behaviour, but maybe the primed cells are hiding away and not circulating.

Thanks again, good to hear all this.

I need to read all the discussion here properly but have been wondering about the reported changes in NK function or talk of ‘exhausted’ NK cells and if this was more a case of them just being different. And on possibly relevowith Fluge and Mella’s work.

Where would they hide? It sounds like hiding in lymphoid tissue is a possibility again, but a lot of the ideas talked about seem hypothetical precisely because it’s difficult to study behaviour or cells in those locations.

There was mention of epigenetic changes, so certain points of the DNA with genes (like those responsible for IFN gamma production) being more exposed, so more readily available for transcription. I wondered if the methylation info from SequenceME could she some light here? Or would we hit the tissue dependency issues again?
AIUI there can be antigen specific behaviour (although maybe this was only in mice?) as well as this wider priming talked about.
One of the papers posted here https://www.s4me.info/threads/power...ller-cell-perspective-2025-sinha-et-al.50337/ I’ll post others in that thread later

 

[Axel]

Could DecodeMe genes found in the same tissues (excluding the brain) have an effect on nearby immune cells? (for exemple BTN2A1 and other candidate genes).