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Interferon-ß Interferes With
Helper T-Cell Proliferation


Pette M, Pette DF, Muraro PA, Farnon E, Martin R, McFarland HF
Neurology 1997 Aug;49(2):385-92
National Institute of Neurological Disorders and Stroke, NeuroImmunology Branch, Bethesda, MD 20892-1400, USA
UI # 97416616
Abstract

Interferon-beta (IFN-ß) has beneficial effects on the frequency and severity of relapses, as well as on disease progression in patients suffering from Relapsing/Remitting Multiple Sclerosis.

Its mode of action, however, is not completely understood.

Previous studies on T-Lymphocyte bulk cultures and T-Lymphocyte lines with specificity for different Antigens suggested that the drug might partially act via suppression of T-Cell proliferation and secretion of ProInflammatory Cytokines like Interferon-gamma (IFN-gamma) and/or Tumor Necrosis Factor-alpha (TNF-alpha).

In this study we investigated the effects of human recombinant IFN-ß 1b on proliferation, Interleukin 2 (IL-2) receptor (IL-2R) alpha-chain upregulation, and Cytokine and Chemokine secretion of Myelin Basic Protein-reactive, MS patient-derived T-Cell clones secreting T-Helper Type 1 (Th1) Cytokines.

IFN-ß partially suppressed both Antigen- and IL-2-driven proliferation of these cells without affecting the expression of either IL-2 or IL-2R alpha-chain.

There was no inhibitory effect on the secretion of IFN-gamma, TNF-alpha, and Macrophage Inflammatory Protein (MIP)-1 alpha, but release was rather slightly enhanced.

In conclusion, while IFN-ß does reduce proliferation of Th1-like, MBP-specific T-Cells in vitro, the drug does not result in overall dysfunction of these cells.

Therefore, the effect of IFN-ß on MS may not depend on a primary inhibition of potentially Encephalitogenic T-Lymphocytes.



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