Rouwette
M, Somers K, Govarts C, De Deyn PP, Hupperts R, Van Wijmeersch B, De
Jong BA, Verbeek MM, Van Pesch V, Sindic C, Villar LM, Alvarez-CermeƱo
JC, Stinissen P, Somers V. Novel cerebrospinal fluid and serum autoantibody targets for Clinically Isolated Syndrome. J Neurochem. 2012 Sep 7. doi: 10.1111/jnc.12005. [Epub ahead of print]
Limited information is available on the identity of antigens targeted by
antibodies present in cerebrospinal fluid (CSF) of patients with
Clinically Isolated Syndrome (CIS). The aim of this study was to
identify novel antigens for CIS and investigate their prognostic
potential to predict conversion to Multiple Sclerosis
(MS). We applied Serological Antigen Selection (SAS) to identify
antigens interacting with antibodies present in the pooled CSF from 4
CIS patients, who developed MS. Antibody reactivity towards CIS antigens
identified by SAS was tested in CSF and serum from patients with CIS
(n=123/n=108), MS (n=65/n=44) and other (inflammatory) neurological
diseases (n=75/n=38) as well as in healthy control sera (n=44). Using
SAS, a panel of 6 novel CIS candidate antigens was identified. CSF
antibody reactivity was detected in both CIS and Relapsing-Remitting
(RR) MS. Serum reactivity was significantly increased in CIS and RR-MS
as compared to controls (p=0.03). For 2 antigens, the frequency of
antibody positive patients was higher in CIS patients who converted to
MS as compared to CIS patients without conversion. We identified novel
CIS antigens to which antibody reactivity was primarily detected in CIS
and RR-MS as compared to controls. Possible prognostic potential could
be demonstrated for 2 antigens
This study made a expression library which means you make take the activated genes from the tissues and use bacteri to express the proteins that would be made, of proteins from chronic MS lesions and normal appearing white matter. They then looked at antibodies from 4 people with clinicall ioslated syndrome who then went on to get MS and saw what the antibodies reacted to. We got some new target molecules on was Host cell factor 1 regulator 1 which controls the movement of host cell factor 1 in the cell and this controls transcription of Herpes virus among other things. Others may be against other targets like bestrophin 1. reactivity to these were present in CIS and RRMSers. Is this causal or a response to tissue damage? I think it shows further that MSers can react to a lot of diffeent things in the brain and I know that some of these antibody responses will not be good for you.
Labels: Autoimmuity, CIS