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Immunopathogenesis of Demyelinating Diseases Introduction

It is more than fifty years since the observation of persistently raised immunoglobulin-albumin ratios in the cerebrospinal fluid of the majority of multiple sclerosis (MS) patients alerted clinicians and scientists to the immunopathogenic nature of the disease. Recognition of the oligoclonal nature of the immunoglobulin G, and the discovery of the association of disease susceptibility with certain haplotypes of the major histocompatibility complex (MHC) and other immunologically relevant genes have raised the stakes in the search for a putative “MS antigen,” and for possible immune mechanisms involved in the generation of MS lesions. Specifically, the tantalizing evidence that experimental autoimmune inflammatory demyelination can be induced by CD4 T lymphocytes with myelin protein-specific antigenicities, in particular for myelin basic protein, has spawned a wealth of data on cellular immunity in MS. Now, neuroimmunologists are faced with a number of questions which include: 1. What and where is the origin of the demyelinating autoimmune response? Is it primarily within the brain, or is it located in the immune system? 2. Which is the target autoantigen? Is there any autoantigen common to all cases of MS, or could there be different target structures in different individuals? Should we focus solely on myelin components, or should other brain proteins be included in our search as well? What is the immune status of the brain? How far is it connected to the peripheral immune system, and what is the role of the protective bloodtissue barriers? Which genes are actually contributing to susceptibility to inflammatory demyelinating diseases? Which “susceptibility genes” are expressed in the brain, which ones in the immune system? Will the unexpected diversity of lesion patterns distinguishing individual MS cases provide a clue to corresponding diversity of pathogenic factors in MS? 6. Although spontaneous remyelination within MS plaques is deplorably modest, it can be enhanced therapeutically. How will we be able to make use of growth factors, or polycional immunoglobulins to enhance regenerative mechanisms? 3.