Showing papers by "Marco Salvetti published in 1994"
TL;DR: The hypothesis that the described associations are due to linkage disequilibrium with an undetected polymorphism of a primarily involved linked locus is supported.
Abstract: Many autoimmune diseases have been shown to be associated with genes in the HLA region. In some cases, e.g., coeliac disease (CD), insulin-dependent diabetes (IDDM), narcolepsis, the degree of association with polymorphism at a given locus is so strong (relative risks of 10 or more, presence of the marker in more than 90% of the patients) that the locus can plausibly be assumed to be involved in the pathogenesis. In other cases, the degree of association is much lower, as in the three diseases considered in the present study: systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS). The HLA alleles most significantly associated, DR3 in SLE, DR4 in RA, and DR2 in MS, show relative risks around 3 and are present, typically, in only 30%-50% of the patients. This allows the hypothesis that the described associations are due to linkage disequilibrium with an undetected polymorphism of a primarily involved linked locus. Consequently, the search for more strongly associated polymorphisms is actively pursued whenever new loci in the HLA region are identified, especially when these loci participate in the control of the immune response. The HLA genes controlling heat shock proteins
19 citations
3 citations
TL;DR: It seems that infiltrating, blood-born macrophages are the major source of NO in the CNS during EAE, and treatment of EAE with NOsynthase inhibitors, either intraperitoneally or intraventrieularly, resulted in a marked aggravation of the disease.
1 citations
01 Jan 1994
TL;DR: Myelin basic protein, a major myelin antigen, is considered a potential target of the immunopathologic process in Multiple Sclerosis and the T cell response against this self-antigen is being extensively investigated in patients with MS.
Abstract: Myelin basic protein (MBP), a major myelin antigen, is considered a potential target of the immunopathologic process in Multiple Sclerosis (MS). MBP-specific T lymphocytes indeed mediate experimental allergic encephalomyelitis, the animal model of MS. Furthermore in vivo- activated T cell clones reactive to MBP were detected in the peripheral blood of patients, but not of healthy individuals (1). For these reasons the T cell response against this self-antigen is being extensively investigated in patients with MS.