MYELIN PROTEIN EXPRESSION IS INCREASED IN LYMPH-NODES OF MICE WITH RELAPSING EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS

Citation
Aj. Mackenziegraham et al., MYELIN PROTEIN EXPRESSION IS INCREASED IN LYMPH-NODES OF MICE WITH RELAPSING EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS, The Journal of immunology, 159(9), 1997, pp. 4602-4610
Citations number
42
Journal title
ISSN journal
00221767
Volume
159
Issue
9
Year of publication
1997
Pages
4602 - 4610
Database
ISI
SICI code
0022-1767(1997)159:9<4602:MPEIII>2.0.ZU;2-B
Abstract
Myelin proteins had been thought to be sequestered behind the blood-br ain barrier, Recently, however, myelin proteins have been found to be expressed in lymphoid tissues, The myelin basic protein (MBP) gene is embedded within a larger transcription unit called the golli-MBP gene, This larger gene encodes both the ''classic'' MBPs as well as the str ucturally related golli-MBPs. In this study, golli-MBP expression in l ymph nodes was examined in four different models of relapsing experime ntal autoimmune encephalomyelitis (rEAE), Disease in these rEAE models was induced by the adoptive transfer of T lymphocytes specific for 18 .5-kDa MBP, MBP peptide 83-102, or PLP peptide 139-151 in the SJL/J mo use and the adoptive transfer of T lymphocytes specific for MBP peptid e Ac1-9 in the (SJL/J x PL/J)F-1 mouse, In all four models, expression of golli-MBP BG21 mRNA was Increased two-to fivefold in lymph nodes o f mice 45 to 60 days post-transfer, Immunohistochemical analysis indic ated that expression occurred principally in macrophages within lymph nodes, Endogenous golli-MBP epitopes within lymph node cells stimulate d ''classic'' MBP 1-44-specific T lymphocytes, and his stimulatory abi lity resided within the adherent lymph node cell population, An increa se in myelin protein expression within lymph nodes during rEAE has imp lications with regard to intra-and intermolecular epitope spreading. T his is the first report describing an increase in ''target autoantigen expression within lymphoid tissue during all autoimmune disease.