T-CELLS WITH ENCEPHALITOGENIC POTENTIAL FROM MULTIPLE-SCLEROSIS PATIENTS AND LEWIS RATS FAIL TO INDUCE DISEASE IN SCID MICE FOLLOWING INTRACISTERNAL INJECTION

Intracisternal (IC) transfer of cerebrospinal fluid (CSF) mononuclear cells from multiple sclerosis (MS) patients has been reported by other s to induce an 'MS-like pathology' in severe combined immunodeficient (SCID) mice. We injected cells from several sources intracisternally i nto SCID mice and assessed the recipients for clinical and histologica l disease. CSF cells and myelin basic protein (BP)-specific T lymphocy tes from MS patients failed to induce clinical or histological disease following IC injection in SCID mice. Similarly, encephalitogenic BP-s pecific T cells from Lewis rats were unable to induce disease after IC injection in either SCID mice or Lewis rats, even at cell numbers whi ch induced experimental autoimmune encephalomyelitis in Lewis rats fol lowing intraperitoneal (IF) injection. In contrast, naive Lewis rat sp lenocytes, which were capable of inducing lethal graft-versus-host (GV H) disease following IP transfer in SCID mice, induced paralysis and h istopathological changes following IC transfer in SCID mice. We conclu de that MS CSF cells do not typically transfer disease into SCID mice following IC injection. Furthermore, it appears likely that neuropatho logical disease following IC transfer of cells reflects the potential of the transferred cells for inducing GVH disease. Specific recognitio n of neuroantigens by T cells, as occurs in EAE, is probably not invol ved in the transfer of paralytic disease by IC transferred MS patient CSF cells.