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Protein regulator may play inflammation role


A new study describes a protein regulator known as Trabid as an important piece of the puzzle that leads to autoimmune inflammation of the central nervous systems in multiple sclerosis patients. Researchers believe that Trabid and Jmjd2d may be potential therapeutic targets for the treatment of inflammatory diseases such as MS.

Researchers, led by Shao-Cong Sun, professor of Immunology at the University of Texas MD Anderson Cancer Center, found that deletion of a protein-coding gene known as Zranb1, which encodes Trabid, in dendritic cells inhibited expression of IL-12 and IL-23, impairing differentiation of inflammatory T-cells. The process protected study mice from autoimmune inflammation.

Cytokines are small proteins important for cell signaling, and IL-12 and IL-23 are mediators of inflammation and associated with inflammatory diseases. Pro-inflammatory cytokines like IL-12 and IL-23 connect innate responses and immune responses and are also involved in autoimmune and inflammatory diseases, said the researchers. The innate immune system, also known as the nonspecific immune system, is an important subsystem of the overall immune system that comprises the cells and mechanisms that defend the host from infection by other organisms.

Study results were published in the online issue of Nature Immunology.

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