P. Bongioanni et al., Decreases in T-cell tumor necrosis factor alpha binding with interferon beta treatment in patients with multiple sclerosis, ARCH NEUROL, 56(1), 1999, pp. 71-78
Objective: To investigate the effects of interferon beta treatment on T-cel
l tumor necrosis factor alpha (TNF-alpha) binding (which is a possible mark
er for T-cell-dependent immune function) in patients with multiple sclerosi
s.
Design: The TNF-alpha binding on T lymphocytes from patients with stable re
lapsing-remitting multiple sclerosis was assayed before and 3 and 6 months
after the start of treatment with interferon beta.
Setting: The study was performed on ambulatory patients in a tertiary care
center.
Patients: Eighteen patients with clinically definite stable relapsing-remit
ting multiple sclerosis (13 women and 5 men; mean [+/- SD] age, 32.6 +/- 7.
1 years) were selected consecutively. Clinical status was defined according
to the Expanded Disability Status Scale. All patients were treated with 8
X 10(6) U of interferon beta-1b subcutaneously every other day. Eighteen ag
e- and sex-matched healthy subjects, with no family history of neuropsychia
tric disorders, served as controls.
Results: T lymphocytes from untreated patients with multiple sclerosis had
significantly more TNF-or receptors than those from controls (mean +/- SE,
837 +/- 33 vs 135 +/- 5 receptors per cell). After 3 months of treatment wi
th interferon beta-1b, they showed a significant decrease (P<.001) in TNF-a
lpha binding (452 +/- 29 receptors per cell). After 6 months, T-cell TNF-al
pha maximal receptor numbers were even lower (345 +/- 35 receptors per cell
).
Conclusion: Given that increased TNF-alpha binding might be linked to lymph
ocyte activation, our data demonstrate that a major effect of interferon be
ta-1b treatment is to decrease T-cell activation.