A simplified program operative during transition of lymphocytes and monocytes through cerebral endothelium and ependyma might provide an effective mechanism promoting reversal of roles of these two cell types with regard to antigen reactivity and antigen presentation. One might envision a role for the oligodendrocyte that mirror images injury to myelin-invested axons as an initiating mechanism in both presenting antigen and in determining the establishment of endless cycles of amplified demyelination. These appear paradoxically dictated by dynamics of the cyclical remyelination of such initially injured axons. Neuroinflammation with involvement of axons would progress as evolving demyelinative plaques scattered in random fashion in white matter.  Macrophages appear to act as effector cells in demyelination of inflamed regions that propagate lymphocyte-induced effects in antigen presentation and immune response. Antigen presentation is implicated as a mechanism of progression of MS plaques. Demyelination depends on active phagocytosis of myelin lipid, in response to such antigen presentation. Transforming roles of lymphocyte antigen presentation and macrophage reactivity appear central to ongoing demyelination and remyelination cycles superimposed on an inflammatory axonopathy.