Decreases in T-Cell Tumor Necrosis Factor α Binding With Interferon Beta Treatment in Patients With Multiple Sclerosis

This is the authors' abstract. We don't add key points for this paper.

OBJECTIVE: To investigate the effects of interferon beta treatment on T-cell tumor necrosis factor alpha (TNF-alpha) binding (which is a possible marker for T-cell-dependent immune function) in patients with multiple sclerosis. DESIGN: The TNF-alpha binding on T lymphocytes from patients with stable relapsing-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-remitting 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 age- and sex-matched healthy subjects, with no family history of neuropsychiatric disorders, served as controls. RESULTS: T lymphocytes from untreated patients with multiple sclerosis had significantly more TNF-alpha receptors than those from controls (mean+/-SE, 837+/-33 vs 135+/-5 receptors per cell). After 3 months of treatment with interferon beta-1b, they showed a significant decrease (P<.001) in TNF-alpha binding (452+/-29 receptors per cell). After 6 months, T-cell TNF-alpha maximal receptor numbers were even lower (345+/-35 receptors per cell). CONCLUSION: Given that increased TNF-alpha binding might be linked to lymphocyte activation, our data demonstrate that a major effect of interferon beta-lb treatment is to decrease T-cell activation.

Interferon beta-1b was associated with reduced T-cell TNF-alpha binding in stable RRMS; supports immunomodulatory effect but leaves open clinical relevance.