Early Findings on MP in Multiple Sclerosis (MS)

The first clear evidence of an association between MP in circulation and MS disease activity was found by A. Minagar et al. [37]. They found that endothelial MP (EMP) bearing CD31 (PECAM-1) were elevated significantly during exacerbations of RR-MS compared to remissions. In follow-up studies, they observed that MS plasma, but not control plasma, induced formation of EMP-monocyte complexes [38] and that these complexes are a good biomarkers of disease activity in MS [39, 40]. The same group subsequently showed that treatment with interferon 1beta induced reduction of MS-associated EMP in patients [41].

Since autoimmunity may contribute to the etiology of MS, it is of interest that MP-associated autoantigens can form immune complexes with inflammatory potential [42]. Antiphospholipid antibodies (APLA) were reported in MS, leading to a more systematic study of APLA in a series of MS patients, with the unexpected finding that APLA in MS were exclusively IgM class [43].

Evidence of platelet activation in MS was also reported by that group [44]. Since platelet activation is always accompanied by release of PMP, it is likely that the “missing PMP” are being consumed or sequestered in MS or bind to leukocytes. This may apply to Alzheimer’s disease (AD) as well since platelet activation was observed in AD but not elevation of free PMP [45].

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