Evolution of anti-JCV antibody index.

<p>Anti-JCV antibody indices are displayed in seronegative and seropositive patients at the different time points during follow-up. At each visit, the total number of patients, the number of anti-JCV antibody positive patients and their distribution among different index categories are shown. JCV, John Cunningham virus.</p

Spearman correlation between anti-JCV antibody index and patients’ age.

<p>The correlation between the rank of patient's age and the rank of anti-JVC antibody index is visualized, i.e. the Spearman correlation coefficient with its significance.</p

Clinical and baseline demographic data.

<p>Clinical and baseline demographic data.</p

Power to predict stability or change of long-term anti-JCV antibody status.

<p>Power to predict stability or change of long-term anti-JCV antibody status.</p

Percentages of patients switching between different anti-JCV antibody index categories.

<p>(A) Percentage of patients with anti-JCV antibody index ≤0.9 at baseline (n = 66) switching to higher index categories at least once during follow-up. (B) Percentage of patients with positive anti-JCV serostatus and antibody index ≤0.9 at baseline (n = 23) switching to higher index categories at least once during follow-up. (C) Percentage of patients with anti-JCV antibody index >0.9 and ≤1.5 at baseline (n = 19) switching to higher or lower index categories at least once during follow-up. There was no patient remaining within the baseline index category during follow-up. (D) Percentage of patients with anti-JCV antibody index >1.5 at baseline (n = 69) switching to lower index categories at least once during follow-up.</p

Longitudinal change of anti-JCV serostatus.

<p>Frequency of conversion and reversion of anti-JCV serostatus from baseline throughout follow-up.</p

Variables of disease course and their correlation with EDSS outcome 10 years after disease onset

<p>Variables of disease course and their correlation with EDSS outcome 10 years after disease onset</p

time to cognitive dysfunction.

<p>Kaplan-Meier curves of the risk of developing cognitive dysfunction according to disability status 10 years after onset. Log rank test used for calculation of significancy.</p

Baseline clinical and demographic data and their correlation with EDSS outcome 10 years after disease onset

<p>Baseline clinical and demographic data and their correlation with EDSS outcome 10 years after disease onset</p

Cerebrospinal fluid B cells and disease progression in multiple sclerosis - A longitudinal prospective study

<div><p>Background</p><p>There is evidence that B cells play an important role in disease pathology of multiple sclerosis (MS). The aim of this prospective observational study was to determine the predictive value of cerebrospinal fluid (CSF) B cell subtypes in disease evolution of patients with MS.</p><p>Materials and methods</p><p>128 patients were included between 2004 and 2012. Median follow up time was 7.9 years (range 3.3–10.8 years). 10 patients were lost to follow-up. 32 clinically isolated syndrome- (CIS), 25 relapsing remitting MS- (RRMS), 2 secondary progressive MS- (SPMS) and 9 primary progressive MS- (PPMS) patients were included. The control group consisted of 40 patients with other neurological diseases (OND). CSF samples were analyzed for routine diagnostic parameters. B cell phenotypes were characterized by flow cytometry using CD19 and CD138 specific antibodies. Standardized baseline brain MRI was conducted at the time of diagnostic lumbar puncture. Main outcome variables were likelihood of progressive disease course, EDSS progression, conversion to clinical definite MS (CDMS) and relapse rate.</p><p>Results</p><p>CSF mature B cells (CD19+CD138-) were increased in bout-onset MS compared to PPMS (p<0.05) and OND (p<0.001), whereas plasma blasts (CD19+CD138+) were increased in bout-onset MS (p<0.001) and PPMS (p<0.05) compared to OND. CSF B cells did not predict a progressive disease course, EDSS progression, an increased relapse rate or the conversion to CDMS. Likelihood of progressive disease course (p<0.05) and EDSS (p<0.01) was predicted by higher age at baseline, whereas conversion to CDMS was predicted by a lower age at onset (p<0.01) and the presence of ≥9 MRI T2 lesions (p<0.05).</p><p>Conclusion</p><p>We detected significant differences in the CSF B cell subsets between different clinical MS subtypes and OND patients. CSF B cells were neither predictive for disease and EDSS progression nor conversion to CDMS after a CIS.</p></div