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Syngeneic bone marrow transplantation eliminates V β 8.2 T lymphocytes from the spinal cord of Lewis rats with experimental allergic encephalomyelitis
Author(s) -
Burt R. K.,
Burns W.,
Ruvolo P.,
Fischer A.,
Shiao C.,
Guimaraes A.,
Barrett J.,
Hess A.
Publication year - 1995
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/jnr.490410412
Subject(s) - encephalomyelitis , myelin basic protein , bone marrow , immunology , multiple sclerosis , medicine , myelin , transplantation , spinal cord , experimental autoimmune encephalomyelitis , central nervous system , immune system , pathology , psychiatry
Experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis (MS), is a paralytic disease of the central nervous system (CNS) mediated by T‐lymphocytes reactive to myelin basic protein (MBP). Lewis rats actively immunized with fragment 68 to 82 of guinea pig MBP develop a monophasic disease with spontaneous recovery. Lymphocyte recognition of the primary encephalitogenic sequence of MBP (fragment 68 to 82) is V β 8.2 T cell receptor (TCR) skewed [1–3]. Lewis rats in clinical remission at 1 month and 3 months after spontaneous resolution of EAE retain V β 8.2 T‐lymphocytes in the CNS when analyzed by reverse transcriptase polymerase chain reaction or in situ hybridization. In contrast, I and 3 months after clinical remission from syngeneic bone marrow transplantation, V β 8.2 T lymphocytes are absent from the CNS. During clinically active EAE and inflammatory breakdown of the blood‐brain barrier, immune ablation and reconstitution with syngeneic bone marrow results in clinical tolerance of the new immune system to myelin. © 1995 Wiley‐Liss, Inc.