I wish it was computationally plausible to run the anomolous dots receptor shapes (not sequences) through in-silica binding assays to the whole human proteome.
There is probably some reason (other than it being computationally impossible) why this wouldn't be a magic bullet for determining autoimmunity effects.
I think it is computationally impossible because we are talking about recognising something like decamer peptides with 20 amino acid options at each point ( peptide alternatives = 100,000,000,000,000,000,000). What is much worse is that we need to know the binding affinity window involved. Too high binding kills T cells as much as too low bores them. And the peptide has to be recognised in the context of not just the right MHC class II 'tongs' but also CD3, CD4 and all sorts of other co-factors.
My problem is that over a period of 30 years in immunology labs I watched T cell enthusiasts fail consistently in finding any evidence for specific T cell receptor bindings relate to autoimmunity.Either the problem is too difficult or, to my mind more likely, they are irrelevant. Unfortunately many hundreds of millions of dollars have been invested in the idea that T cell receptors are worth exploring.
My sense is that what specific clones recognise may not be very interesting. What may be much more important is skewing of T cell behaviour in a more non-specific way. That might give rise to clonal expansion. But I am still confused about what this paper is about. Clonal expansion is something quite specific about lots of T cells having identical receptors. Lots of T cells having rather similar receptors is something quite different. And lots of T cells recognising the same peptide is again quite different. I am afraid I have not had time to look at the presentation itself but I am confused.