[Immunity and catabolism of nucleic acids: the problem of multiple sclerosis?]

In multiple sclerosis (MS), exogenous or endogenous nucleic acid fragments not (or partially) catabolised inside central nervous system (CNS) could entertain an inflammatory and even demyelinating process, and delay resynthesis of myelin. So, exogenous nucleic acids could act as starting agents for acute phase. Nucleic acid material can be released by the enzymes of nucleic acid catabolism and by the antibodies to nucleic acids possibly synthesized. A preliminary approach of such hypothesis has been made by study of cerebrospinal fluid ribonuclease activity and intrathecal synthesis of antibodies to nucleic acids. These two factors are significantly different in MS and in infectious processes of CNS groups. According to our hypothesis MS could arise from a genetic defect of oligodendrocyte (ODC) acting in genome expression and consequently leading to the persistence of nucleic acid fragments. This defect of ODC might be associated to another immune defect explaining various evolutive forms of the disease.