In vivo adoptive transfer of CD4+ T helper cell type 1 clones reactive with autologous myelin basic protein (MBP) may initiate an inflammatory demyelinating disease of the central nervous system called experimental autoimmune encephalomyelitis. Although MBP is also a component of peripheral nervous system (PNS) myelin, previous studies have failed to demonstrate inflammation in the PNS induced by MBP-reactive T cells. Here, we report on two MBP-specific T cell clones that preferentially initiate inflammatory and demyelinating peripheral neuritis when adoptively transferred to syngeneic recipients. The MBP epitope recognized by these clones spans the junction of exons 6 and 7 and, therefore, is present in the 21- and 18.5-kD but not the 14- and 17-kD MBP isoforms, in which exon 5 is spliced to exon 7. The data suggest that MBP may be processed and presented differently in the central nervous system and PNS, and they provide evidence for MBP as a potential target for autoimmune reactions in the PNS.
Article|
August 01 1995
Experimental autoimmune peripheral neuritis induced in BALB/c mice by myelin basic protein-specific T cell clones.
S Abromson-Leeman,
S Abromson-Leeman
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
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R Bronson,
R Bronson
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
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M E Dorf
M E Dorf
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
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S Abromson-Leeman
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
R Bronson
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
M E Dorf
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1995) 182 (2): 587–592.
Citation
S Abromson-Leeman, R Bronson, M E Dorf; Experimental autoimmune peripheral neuritis induced in BALB/c mice by myelin basic protein-specific T cell clones.. J Exp Med 1 August 1995; 182 (2): 587–592. doi: https://doi.org/10.1084/jem.182.2.587
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