ABSTRACT
I. INTRODUCTION To understand how interferon-0 (IFN-0) acts to influence the course of multiple sclerosis, one has to consider several biological levels of its activity. In this Chapter, I focus on a level at the very basis of any complex phenotype: how genes are turned on or off to express or repress their products, ultimately causing an altered behavior of cells and an entire organism. Although we do not precisely know the mechanism by which IFN-/3 influences the course of multiple sclerosis, it is next to certain that regulating gene expression is a major component. This assumption is based on what we have learned in two decades of molecular IFN research, the finding that none of the changes in cells IFNs are known to elicit, be it the antiviral response, the altered growth or differentiation behavior, or the modulated functions of cells within the immune system, are possible without changing the levels of gene products by directly regulating their transcription. Additional ways of regulating gene expression through the control of mRNA processing or translation exist but will not be considered here, because their relevance to the IFN biology is not yet well understood.
