Abstract
Lymphocytic choriomeningitis virus (LCMV) induces a chronic, wasting syndrome when injected intracerebrally into H-2b mice homozygous for a β2-microglobulin (β2-m (-/-)) gene disruption. These mice have very few CD8+ T cells and express little class I MHC glycoprotein, though minimal levels of the H-2Db molecule have been detected on in vitro cultured β2-m (-/-) cells. The inderlying immunopathological process in these β2-m (-/-) mice is mediated by virus immune CD4+ effectors. However, adoptively transferred CD8+ T cells from normal, LCMV-infected H-2Db compatible donors induce significant (but low level) meningitis in β2-m (-/-) recipients. Such mice develop neither the neurological disease characteristic of LCM nor the persistent, though generally non-fatal, debility that occurs when only the CD4+ T cell subset is involved.
Original language | English (US) |
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Pages (from-to) | 11-17 |
Number of pages | 7 |
Journal | Journal of Neuroimmunology |
Volume | 46 |
Issue number | 1-2 |
DOIs | |
State | Published - Jul 1993 |
Keywords
- Debility caused by CD4 T cells
- Immunopathology
- Meningitis
- T cell specificity
- T cell targeting