Inflammation is an important component of the body's response to infection and tissue damage, but uncontrolled inflammation can lead to various diseases and promote cancer formation.
A new study led by the University of Texas MD Anderson Cancer Center found that a protein regulatory factor called Trabid is an important part of the autoimmune inflammation of the central nervous system in patients with multiple sclerosis.
The proinflammatory cytokines interleukin 12 (IL-12) and IL-23 connect innate responses and adaptive immune responses. They are also involved in autoimmune and inflammatory diseases. When the researchers deleted Zranb1 (which encodes Trabid) in dendritic cells, the induction of the expression of IL12 and IL23 by Toll-like receptors (TLRs) was inhibited. This impaired the differentiation of inflammatory T cells and protected mice from autoimmune inflammation. Trabid facilitated TLR-induced histone modifications at the promoters of IL12 and IL23, which involved deubiqutination and stabilization of the histone demethylase Jmjd2d.
“ Our findings highlight an epigenetic mechanism for the regulation of IL12 and IL23 and establish Trabid as an innate immunological regulator of inflammatory T cell responses.” the researchers said.
Trabid and Jmjd2d may be potential therapeutic targets for the treatment of inflammatory diseases such as multiple sclerosis.
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