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Active and passive experimental autoimmune encephalomyelitis in strain 129/J (H‐2 b ) mice
Author(s) -
Fritz R.B.,
Zhao M.L.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19960815)45:4<471::aid-jnr17>3.0.co;2-3
Subject(s) - experimental autoimmune encephalomyelitis , myelin basic protein , myelin proteolipid protein , immunology , adoptive cell transfer , active immunization , encephalomyelitis , peptide , immunization , myelin , strain (injury) , autoimmune disease , multiple sclerosis , medicine , antigen , biology , t cell , immune system , central nervous system , antibody , biochemistry
Failure of C57BL/6J and C57BL/10Sn (H‐2 b ) mice to exhibit clinical signs of experimental autoimmune encephalomyelitis following immunization with myelin basic protein (MBP) has been interpreted to indicate that mice of this haplotype are resistant to EAE. Recently, we immunized strain 129/J (H‐2 b ) mice with rat MBP and found that clinical signs of EAE were expressed in the majority of animals within 2 to 3 weeks. Passive EAE was readily induced by adoptive transfer of MBP‐specific T cell lines to syngeneic recipients. MBP peptide 89–101 and PLP peptide 178–191 induced EAE upon active immunization although proteolipid protein peptide 139–151 was ineffective in this regard. Strain 129/J mice never recovered fully from acute EAE, and signs of relapsing disease were not observed. © 1996 Wiley‐Liss, Inc.