Genetics: BTN2A2 and BTN3A3

It would all fit together nicely. But then there always seems to be a way to fit things together nicely. I think Jackie Cliff is pleased the way data are coming out.

I am reminded of the film Amelie. If some set of T cells are causing trouble they are doing it in a very surreptitious way. Nobody can see where they are or what they are doing. Things turn up in research data but we cannot see how they got there or who they belong to. Maybe the writing on the wall is part of the story. Like the photos in the booths in Amelie.

Maybe one could image patterns of writing attached to TGF beta binding proteins on matrix and read what messages the T cells or macrophages have left there.
 
Jonathan Edwards said:
Maybe one could image patterns of writing attached to TGF beta binding proteins on matrix and read what messages the T cells or macrophages have left there.
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Are you talking about the kind of biopsies you describe here?

Jonathan Edwards said:
The first step would be to look at patterns of adsorbed signalling proteins on matrix fibres using biopsies and immunochemistry. Calibrating between individuals would probably be hard. I would look for changes in patterns. One the the best bits of evidence for our rheumatoid theory was that the immunoglobulin receptor CD16 is expressed on macrophages and adsorbed on to elastic fibres at exactly the site where rheumatoid nodules occur. I would not expect anything quite as clear-cut as that for ME/CFS but something equally striking might turn up around muscle or something.

Taking biopsies is not easy but if one knew exactly what was looking for a fairly small series might provide a very useful clue.
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And if so do you expect any studies like this to happen in this new post-DecodeME landscape? You mentioned Wusts group as a possibility further down that thread.
 
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