Summary of Zelek, W. et al; Measurement of soluble CD59 in CSF in demyelinating disease: evidence for an intrathecal source of soluble CD59. Mutiple Sclerosis, Feb 2018. Click here for the full article.

Activation of complement via the classical, lectin or alternative pathway leads to the formation of C3 convertase complexes that cleave C3 to C3a and C3b. C3b causes C5 convertase, which ultimately causes formation of the membrane attack complex (MAC) responsible for cell lysis. CD59 regulates formation of MAC by preventing recruitment of C9.

This study investigates the role of sCD59 in patients with demyelinating disorders. Cerebrospinal fluid (CSF) and matching plasma samples were taken from 78 patients with a demyelinating disorder and 34 from healthy controls. The concentration of sCD59 in these samples was measured using the Hycult Biotech sCD59 ELISA (HK374). An interesting finding was that sCD59 levels in CSF were approximately double those in matched plasma. The results further demonstrated that there was no significant difference in sCD59 levels between the various disease groups.

To determine the source of sCD59 in CSF, the study further performed immunohistochemical staining of brain sections. These results demonstrated that the choroid plexus is likely a site of abundant expression in the brain and may be a site of immune activation.

Whether the (relatively) high amounts of sCD59 in CSF are of any functional relevance remains to be demonstrated. In principle, sCD59 might contribute to homeostasis by dampening down complement activation in the CSF, but it is not a biomarker of demyelinating diseases.