| Autor: |
Lavi, Ehud, Constantinescu, Cris S., Ramakrishna, C., Tschen, S., Bergmann, C. C., Stohlman, S. A. |
| Zdroj: |
Experimental Models of Multiple Sclerosis; 2005, p759-769, 11p |
| Abstrakt: |
Pathogenesis induced by mouse hepatitis virus (MHV) infection of rodents is characterized by acute viral encephalomyelitis and demyelination which progresses to a persistent CNS infection associated with ongoing myelin loss, pathologically similar to multiple sclerosis (MS). Although humoral immunity appears redundant for the control of acute virus replication, it is vital in maintaining virus at levels detectable only by RNA analysis. T cell mediated control of acute infection cannot be sustained in antibody (Ab) deficient mice, resulting in virus reactivation. The protective role of Ab during persistence is strongly supported by detection of Ab in the cerebrospinal fluid of MHV infected rodents and maintenance of virus specific Ab secreting cells (ASC) in the CNS long after virus clearance. Ab mediated neutralization constitutes the major mechanism of protection, although fusion inhibition also plays a minor role. Delayed accumulation of ASC, concomitant with a decline in T cell function, assures control of residual virus while minimizing T cell mediated pathology. Although there is little evidence for a detrimental role of Ab in demyelination, an association between Ab mediated protection and remyelination is unclear. [ABSTRACT FROM AUTHOR] |
| Databáze: |
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