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Multiple sclerosis (MS) is a demyelinating disease of the central nervous system of unknown etiology. Based on a hypothesis that MS is caused by certain viral infections, the efficacy of interferon β was examined in patients and it became the first disease-modifying drug (DMD) approximately 30 years ago. Through the series of research utilizing experimental autoimmune encephalomyelitis, many other DMDs were later developed. With emerging insights on limitation of the animal model, newer treatment strategies are being developed based on pathological findings from MS patients. In the current article, the history of MS treatment and its future prospects will be reviewed and discussed.

To accommodate the vast antigenic exposure from both food components and commensal bacteria, the gut has evolved a naturally anti-inflammatory environment. We have recently shown that lactic acid bacteria (LAB), a major population of small intestinal microbiota and often found in fermented foods, contain a large amount of double-stranded RNA and capable of inducing interferon-β (IFN-β) production from dendritic cells (DCs) via the Toll-like receptor 3 (TLR3) pathway. It is a significant feature of LAB and was not observed in other bacteria tested. Moreover, IFN-β secreted in response to LAB prevented experimental colitis. These results identify TLR3 as a sensor to small intestinal commensal bacteria and contribute to anti-inflammatory mechanism. We also show that oral administration of β-glucan enhance intestinal and systemic immune response in dectin-1-dependent manner. Thus elucidation of "gut to systemic immune-homeostasis" mediated by innate signals will be valued for the development of gut-biology and science-based food immunology, with a focus on innovation in the health and medical industries.

Following the completion of the Human Genome Project in 2003, we were able to clarify the comprehensive profile of the whole human genome on DNA microarray. KeyMolnet is a bioinformatics tool for analyzing molecular interactions on the curated knowledge database. It promotes genome-based drug discovery research aimed at mining the most relevant molecular target to personalized medicine. Multiple sclerosis (MS) is an inflammatory demyelinating disease with a relapsing-remitting clinical course, affecting exclusively the human central nervous system white matter. By DNA microarray, we identified a set of differentially expressed genes in T lymphocytes between MS and healthy subjects, and between acute relapse and complete remission. Hierarchical clustering of discriminator genes established the molecular classification of MS subgroups, associated with the therapeutic response to interferon-beta. The molecular network of the genes involved in development of MS and induction of acute relapse of MS was related to NF-kappaB-regulated gene expression. Prion diseases are an intractable neurodegenerative disease, mediated by an abnormal prion protein PrPSc. The protein conformational conversion from the cellular prion protein PrPC to PrPSc requires an as yet unidentified species-specific chaperone named "Protein X". By protein microarray, we identified a set of novel PrPC interactors, serving as the candidate for X. The molecular network of PrPC and interactors was closely associated with signaling pathways essential for cell survival, differentiation, proliferation and apoptosis. Thus, the molecular network analysis is highly valuable to extract biological implications from a huge amount of microarray data.