B7-H3 (CD276) is a molecule with co-stimulatory function. This means that it is not part of the direct contact between a T cell and its target which involves interaction of the T cell receptor and the target presented by a macrophage (the activation-the stimulatory step), which is required to stimulate the T cell, but an addition interaction (co-stimulation) between the T cell and the macrophage that is required to make the activations step cause multiplication of the T cell. Without it they are switched off. The firs of these co-stimulatory molecules was B7-1 (CD80) and B7-2 (CD86) which interacts with CD28 and CD152. The B7-H3 is anchored into the cell membrane but it can also be cleaved and shed into the fluid outside cells and get into the blood and this is called soluble B7-H3. This can inhibit some immune functions and so it is consistent with the observation that with lower sB7-H3 there was more disease activity such that it was lower in Msers than health controls and within MSers it was lower during attacks than in remission. Is this cause or consequnce?
Is this going to be a biomarker, if is the results show significance of only p<0.05 then this is not very likely as there will be too much overlap between groups.
This reminds of a story, we wanted some fresh MSer CSF and also some healthy controls, so whilst we were asking MSers to do this we thought that we should be willing to do this also so Prof G, MouseDoctor II and Myself all volunteered to have this done. However it was not considered ethical, because of doing an unnecessary procedure with risks if it went wrong and so we never got the samples. This is another example what is OK in one country or with one committee, may not be OK in another.