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Expression of major histocompatibility complex class I antigens in the demyelinating twitcher CNS and PNS
Author(s) -
Taniike Masako,
Marcus Jill R.,
Popko Brian,
Suzuki Kinuko
Publication year - 1997
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(19970301)47:5<539::aid-jnr9>3.0.co;2-i
Subject(s) - microglia , antigen , biology , demyelinating disease , major histocompatibility complex , immunology , cd8 , myelin , mhc class i , mhc class ii , central nervous system , microbiology and biotechnology , inflammation , multiple sclerosis , neuroscience
The expression of the major histocompatibility complex Class I antigens (Class I) was investigated in the nervous system of twitcher (C57BL/6J‐twi), a murine model of Krabbe disease in humans. Class I mRNA expression was low in wild type and in twitcher mice prior to the onset of demyelination. However, immunoreactivity for Class I antigens was demonstrated in the spindle‐shaped cells in the sciatic nerve and in ramified microglia, endothelial cells and Bergmann glia. In twitcher, transcription of Class I mRNA increased significantly with the progression of demyelination and Mac‐1 + macrophages/microglia express Class I immunoreactivity. Class I immunoreactivity was also found in CD3 + T‐cells that were scattered in demyelinating lesions. CD8 + or CD4 + cells were also found in the demyelinating area. The results of this study indicate that immunoreactivity to Class I antigens is detected in certain cells even in the wild‐type mice and that Class I expression is enhanced in the twitcher nervous system paralleling the progression of demyelination. Expression of MHC molecules in non‐immunological demyelinating disease such as twitcher may suggest a role of Class I molecules in the progression of demyelination. Alternatively, the expression may be a non‐specific cellular response to the breakdown of myelin. © 1997 Wiley‐Liss Inc.