| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T49 |
0-451 |
Epistemic_statement |
denotes |
For example, disruption of MHC class I function by deletion of β 2 -microglobulin in SJL/J mice results in more demyelination and increased neurological deficit (Begolka et al., 2001) , and in the SJL/J strain it has been suggested that MHC class II-restricted T-cell response (Miller et al., 1987) , and epitope-spreading to myelin antigens may be the mechanism of demyelination and neurological deficit (Croxford et al., 2002; Miller et al., 1997) . |
| T50 |
452-709 |
Epistemic_statement |
denotes |
However, CD8 + MHC class I-restricted cytotoxic T-cells have definitely been implicated in human MS, and it is likely that demyelination and neurological dysfunction in humans are a combination of both CD8 + -and CD4 + -mediated mechanisms (Neumann, 2003) . |
| T51 |
710-896 |
Epistemic_statement |
denotes |
Recent pathological studies have shown that CD8 + T-cells may be the most common subset of T-cells in the MS brain and appear to be clonally expanded in MS lesions (Babbe et al., 2000) . |
| T52 |
897-1235 |
Epistemic_statement |
denotes |
Recent experiments in collaboration with Hans Lassmann have demonstrated intense expression of MHC class I in oligodendrocytes, neurons, axons, and astrocytes in the MS lesion (Hoftberger et al., 2003) , and autopsy studies have demonstrated that CD8 + T-cells are statistically associated with axonal injury in MS (Bitsch et al., 2000) . |
| T53 |
1236-1542 |
Epistemic_statement |
denotes |
In addition, CD8 + T-cells have been shown to injure neurons and transect axons in vitro (Medana et al., 2000 (Medana et al., , 2001 , and imaging studies have indicated that axonal loss in MS is a direct correlate for disability (Narayanan et al., 1997; Truyen et al., 1996; van Waesberghe et al., 1999) . |
| T54 |
1543-1663 |
Epistemic_statement |
denotes |
These studies suggest that CD8 + T-cells may be the primary effectors for axonal injury and neurological deficits in MS. |
