Multiple Sclerosis Journal - October 2017 - 1482

Multiple Sclerosis Journal 23(11)
Table 1. Patient population and demographic data.
Stable RRMS

N = 110

%

Female:male
Median age (years)
Median EDSS
Median MSSS
Median disease
duration (years)
Median time on/off
treatment (days)
Treatment with
natalizumab
Treatment with
fingolimod
Treatment with
glatiramer acetate
Treatment with
beta-interferon
Off treatment

86:24
44
2.8
3.45
11.8

78:22

Range
23-65
0.0-7.5
0.03-9.09
0.6-38

887

31-6971

31

28.2

Figure 2. Total lymphocyte count and NK (CD56) cell
count off treatment and on treatment.

24

21.8

15

13.6

NAT: natalizumab; FING: fingolimod; GA: glatiramer acetate;
IFN: beta-interferon.
***p ⩽ 0.001 versus no treatment.

22

20

18

16.4

RRMS: relapsing-remitting multiple sclerosis; EDSS:
Expanded Disability Status Scale; MSSS: Multiple Sclerosis
Severity Scale.18

Table 2. Clinical outcomes including MRI parameters.
Outcome parameters
stable RRMS

n = 110

%

NEDA:NEDA criteria not
fulfilled
No NEDA status as no
MRI data
MRI progression
EDSS progression
Relapse

42:64

38.2:58.2

4

3.6

32
19
47

29.1
17.8
42.7

RRMS: relapsing-remitting multiple sclerosis; NEDA: No
Evidence of Disease Activity; MRI: magnetic resonance
imaging; EDSS: Expanded Disability Status Scale.

and only 3.6% (4 patients) had no MRI imaging in the
observation period.

Analysis of CD56 counts under different
treatments
Our analysis revealed statistically significant differences within NK population on treatment compared
to off treatment (p = 0.001). Post hoc testing showed
circulating NK cell numbers were more than twice
as high on natalizumab (p < 0.001; Figure 2).
Proportions of NK subsets within the raised lymphocyte count did not differ significantly for natalizumab compared to patients off treatment. The
1482

fingolimod group demonstrated a fivefold higher
proportion of NK cells within a suppressed lymphocyte count (p < 0.001; Figure 3). The proportion of
CD56 bright NKs within the total NK cell count was
almost halved (p = 0.011) and the proportion of
CD56 dim NKs increased accordingly (p = 0.011;
Figure 4). The proportion of CD56 bright was
increased on beta-IFN (p = 0.012) with reciprocal
decrease in CD56 dim. No significant changes could
be demonstrated for glatiramer acetate (Figure 5).

Analysis of treatment response
Given that we had previously shown CD56 subsets to
vary significantly between treatment groups, we
included treatment as a fixed factor covariate in each of
the GLM ANOVA models in addition to age and sex.
Table 3 shows the ANOVA results for all CD56 subsets
and the four clinical outcomes. Significant associations
for several CD56 subsets with MRI activity were
observed (p < 0.05). These persisted even when the two
patients with only MRI brain imaging were excluded
from the analysis. There were no associations detected
for NEDA, EDSS progression or relapses (Table 3).
A lower mean of circulating NK cells as well as NK
cell proportion appeared to be associated with stable
MRI imaging (Table 4). Increased bright NK proportion and decreased dim NK proportion within the NK
cell count were also associated with no MRI activity.
This could also be shown for decreased total mean of
dim NK cell count, but not for an increased mean of
the total number of bright NK cells.
Discussion
In this study, we correlated NK cells and their subsets in MS patients with clinical and radiological
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Table of Contents for the Digital Edition of Multiple Sclerosis Journal - October 2017

Contents
Multiple Sclerosis Journal - October 2017 - Cover1
Multiple Sclerosis Journal - October 2017 - Cover2
Multiple Sclerosis Journal - October 2017 - Contents
Multiple Sclerosis Journal - October 2017 - ii
Multiple Sclerosis Journal - October 2017 - iii
Multiple Sclerosis Journal - October 2017 - 1436
Multiple Sclerosis Journal - October 2017 - 1437
Multiple Sclerosis Journal - October 2017 - 1438
Multiple Sclerosis Journal - October 2017 - 1439
Multiple Sclerosis Journal - October 2017 - 1440
Multiple Sclerosis Journal - October 2017 - 1441
Multiple Sclerosis Journal - October 2017 - 1442
Multiple Sclerosis Journal - October 2017 - 1443
Multiple Sclerosis Journal - October 2017 - 1444
Multiple Sclerosis Journal - October 2017 - 1445
Multiple Sclerosis Journal - October 2017 - 1446
Multiple Sclerosis Journal - October 2017 - 1447
Multiple Sclerosis Journal - October 2017 - 1448
Multiple Sclerosis Journal - October 2017 - 1449
Multiple Sclerosis Journal - October 2017 - 1450
Multiple Sclerosis Journal - October 2017 - 1451
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Multiple Sclerosis Journal - October 2017 - 1453
Multiple Sclerosis Journal - October 2017 - 1454
Multiple Sclerosis Journal - October 2017 - 1455
Multiple Sclerosis Journal - October 2017 - 1456
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Multiple Sclerosis Journal - October 2017 - 1464
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Multiple Sclerosis Journal - October 2017 - 1500
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Multiple Sclerosis Journal - October 2017 - 1534
Multiple Sclerosis Journal - October 2017 - 1535
Multiple Sclerosis Journal - October 2017 - 1536
Multiple Sclerosis Journal - October 2017 - 1537
Multiple Sclerosis Journal - October 2017 - 1538
Multiple Sclerosis Journal - October 2017 - 1539
Multiple Sclerosis Journal - October 2017 - 1540
Multiple Sclerosis Journal - October 2017 - 1541
Multiple Sclerosis Journal - October 2017 - 1542
Multiple Sclerosis Journal - October 2017 - 1543
Multiple Sclerosis Journal - October 2017 - 1544
Multiple Sclerosis Journal - October 2017 - 1545
Multiple Sclerosis Journal - October 2017 - 1546
Multiple Sclerosis Journal - October 2017 - 1547
Multiple Sclerosis Journal - October 2017 - 1548
Multiple Sclerosis Journal - October 2017 - 1549
Multiple Sclerosis Journal - October 2017 - 1550
Multiple Sclerosis Journal - October 2017 - 1551
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Multiple Sclerosis Journal - October 2017 - 1566
Multiple Sclerosis Journal - October 2017 - Cover3
Multiple Sclerosis Journal - October 2017 - Cover4
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