Multiple sclerosis is a chronic, disseminated inflammation of the central nervous system which is thought to be driven by autoimmune T cells. Genetic association studies in multiple sclerosis and a large number of studies in the animal model of the disease support a role for effector/memory T helper cells. However, the mechanisms underlying relapses, remission and chronic progression in multiple sclerosis or the animal model experimental autoimmune encephalomyelitis, are not clear. In particular, there is only scarce information on the role of central nervous system-invading naive T helper cells in these processes. By applying two-photon laser scanning microscopy we could show in vivo that antigen unexperienced T helper cells migrated into the deep parenchyma of the inflamed central nervous system in experimental autoimmune encephalomyelitis, independent of their antigen specificity. Using flow cytometric analyses of central nervous system-derived lymphocytes we found that only antigen-specific, formerly naive T helper cells became activated during inflammation of the central nervous system encountering their corresponding antigen.
Do we need more….of course we do.
However, in terms of basic science how much do we need to do in EAE, to understand basic biology when we could probably get the same idea by using a less severe model?
Somebody a couple of days ago extolled the virtue of German ethics but for any piece of work you can take a view in favour or against. I know there are many people reading here who are against..
It is very clear that most cells that arrive in the CNS, do so not because of their antigen-specificity, this was shown over thirty years ago. We know theirmigration markers that they make are important and that is why we have natalizumab and fingolimod.
Two photon microscopy (see education) is a powerful tool in science and there is an argument that can be made that new knowledge is being generated.