In the past I had the chance to take part in a study of a german researcher (Gerd Wallukat) who also tested for a lot of these autoantibodies (with another method) and my results were similiar to the celltrend results.
The researcher told me he isn’t a supporter of the celltrend-elisa-test because it only detects the autoantibodies which are there in high numbers and doesn‘t look for the functionality of the autoantibodies. He looked with his method for the functionality of them: In his theory there are possibly autoantibodies who have a main role (like a leading function) and others who are activated because of the main/leading ones.
For example in my case that meant: He found a lot of autoantibodies (even some I never heard of...like nociceptin, PAR1, MAS,...). But when he antagonised the function of the autoantibodies against beta2-adrenergic and the muscarinic2-receptors in the lab, all the other autoantibodies couldn‘t be detected anymore. So, in my case he thinks the beta2-adrenergic and muscarinic2 are the main/leading ones who are possibly activating others.
It‘s a different approach, but I think what is for sure is that the celltrend results are somehow to be taken seriously.