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and IFN
spontaneous gene expression in MS
From the Departments of Immunology (A. Gayo, Dr. Mozo, A. Suárez, and Dr. Gutiérrez) and Neurology (A. Tuñón and Dr. Lahoz), Hospital Central de Asturias, Universidad de Oviedo, Spain.
Address correspondence and reprint requests to Dr. Carmen Gutiérrez, Servicio de Inmunología, Hospital Central de Asturias, Universidad de Oviedo, Julián Clavería s/n, 33006 Oviedo, Spain.
BACKGROUND: Interferon beta (IFNß) lessens the overall frequency of acute attacks in patients with the relapsing-remitting form of multiple sclerosis (RRMS). IFNß may act by decreasing the synthesis of inflammatory cytokines.
OBJECTIVES: To determine whether IFNß-1b treatment had an initial and sustained effect on the in vivo synthesis and secretion of tumor necrosis factor 
(TNF) and IFN
.
METHODS: A highly sensitive reverse-transcriptase PCR technique was used to measure baseline levels of mRNA in freshly isolated cells from patients before therapy and at 3, 6, and 12 months of treatment. Also, protein concentration was measured in serum and in culture supernatants from mitogen-stimulated cells. The authors studied 16 patients, of whom 11 did not have clinical exacerbations, whereas 5 had one clinical relapse each during the study.
RESULTS: Mean values of TNF mRNA levels in the 11 stable patients decreased significantly at 3 and 6 months of treatment in comparison with initial data. After 6 months of therapy, IFNß-1b downmodulated TNF transcripts in the 5 patients who experienced relapse. In this group of patients, TNF levels rose sharply to reach pretreated values at 1 year of IFNß-1b treatment. At the beginning of therapy, 6 patients had high concentrations of serum TNF, which decreased to normal values following IFNß-1b therapy. IFN mRNA expression also diminished after 6 and 12 months of IFNß-1b therapy in the group of stable patients, whereas nonrelevant variations were observed in patients who had one relapse. Initially, patients’ peripheral mononuclear cells secreted diminished amounts of TNF and IFN on PHA + PMA mitogen stimulation in comparison with normal control subjects. After 1 year of therapy, IFNß-1b restored the normal production of TNF, whereas therapy did not restore IFN secretion to control values.
CONCLUSION: IFNß-1b decreases the spontaneous expression of two proinflammatory cytokines.
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