Under normal physiological conditions, these T reg s could either suppress other populations of T-cells which would otherwise be able to induce autoimmune processes, including those involved in the pathogenesis of MS, or they could cause the expansion of a population of specific CD8 ? T-cells which would have an immune repair function. The nature of the epitope or epitopes involved in this postulated process remains unknown but, by analogy with the parallel studies on melanoma mentioned above [10, 11] , it is suggested that key host epitopes involved are coded for by certain human endogenous retroviruses (HERVs) as activation of these has been extensively documented in MS [32, 33] .