Lack of association between IL-1A and IL-1B promoter polymorphisms and multiple sclerosis

Multiple sclerosis is an autoimmune and inflammatory disease of the CNS characterised by recurrent destruction of myelin which results in heterogeneous and unpredictable clinical manifestations. Although the factors able to foster the initial changes leading to CNS demyelination in patients with multiple sclerosis are still unknown, a discrete number of genes are likely to predispose to the occurrence of multiple sclerosis and to influence its clinical variables. Due to the inflammatory nature of the pathogenic mechanisms mediating CNS damage during multiple sclerosis, association studies have been focused on candidate genes coding for immunorelevant molecules. The interleukin (IL)-1 gene cluster (including IL-1A , IL-1B , IL-1RN ), located on the long arm of chromosome 2 (2q12–22; OMIM Database of National Center for Biotechnology Information; www3.ncbi.nlm.nih.gov:80/Omim) and polymorphic in different sites, represents a good target for association studies in multiple sclerosis. IL-1, in fact, has been detected within multiple sclerosis lesions.1 Moreover, lipopolysaccharide stimulated peripheral blood monocytes of patients with multiple sclerosis produce more IL-1α and IL-1β than controls.2 Due to the potential involvement of IL-1α and IL-1β in multiple sclerosis, a genetically determined polymorphic variation in their production may contribute to the occurrence of multiple sclerosis, or modulate its clinical features. Furthermore, we have recently reported the association …