Abstract

β-interferon ( β-IFN) has both pro and anti-inflammatory properties, the balance of which leads to some suppression of disease activity in multiple sclerosis patients. Here, we examine the immunomodulation of neonatal rodent microglia, the principal CNS accessory cell, by β-IFN and consider the interaction of β-IFN and γ-interferon ( γ-IFN). β-IFN and γ-IFN inhibit microglial proliferation. β-IFN antagonises both γ-IFN-induced upregulation of class II expression and the ability of γ-IFN primed cells to mount a respiratory burst. In contrast, β-IFN upregulates microglial Fc receptor expression and augments tumour necrosis factor alpha secretion from suboptimally stimulated microglia.

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