129/Sv mice are resistant to induction of experimental autoimmune encephalomyelitis (EAE) induced with myelin oligodendrocyte glycoprotein peptide (MOG35-55). Mice of this strain lacking the gene coding for the ligand-binding chain of the IFN-γ receptor develop EAE with high morbidity and mortality. Spleen cells from sensitized IFN-γR-/- mice proliferated extensively when stimulated with MOG peptide in culture and produced high levels of IFN-γ and TNF but no detectable IL-4. Transfer of spleen cells from sensitized IFN-γR-/- mice produced EAE in both IFN-γR+/+ and IFN-γR-/- recipients. Disease was severe in IFN-γR-/- recipients and mortality high (77%). Surviving mice remained moribund until termination of the experiments. IFN-γR+/+ recipients developed disease of equal severity, but with no mortality, and recovered significantly. These results indicate that IFN-γ is not essential for the generation or function of anti-MOG35-55 effector cells but does play an important role in down-regulating EAE at both the effector and induction phase of disease.
|Number of pages||5|
|Journal||Journal of Immunology|
|Publication status||Published - 15 Oct 1996|