Cao Xuetao and others found a new surface regulatory mechanism for immune inflammation

。 Immunity
DC is an important class of natural immune cells that play a key regulatory role in activating the body's immune response and maintaining autoimmune tolerance. Once the pathogen is perceived to invade, DC matures and migrates to immune functions such as lymph nodes, and if DC migration disorders occur, DC will over-gather and active in the inflammatory site, leading to excessive inflammation of tissue and even the occurrence of inflammatory diseases. Exploring the regulatory mechanisms of DC migration process is of great significance for understanding DC's regulatory role in natural immunity and inflammation, and for finding potential therapeutic targets for inflammatory diseases caused by DC migration or active abnormalities.
internal migration of DC is jointly regulated by the interaction of the coercion factor and the chemical factor subject. The chimogenic factor CCL19/CCL21 secreted by lymph node substitum cells acts on the chic factor subject CCR7 expressed by mature DC, promoting DC's migration to the T-cell region of lymphatic tissue and initiating and regulating the adaptive immune response mediated by T-cells. At present, there is no understanding of the regulatory mechanism of DC migration, especially the expression changes and role of long-chain non-coding RNA in DC migration and inflammatory diseases have not been reported. Cao Xuetao and Liu Wei, associate professor of the National Key Laboratory of Medical Immunology at naval medical university, found that lnc-Dpf3 played a negative regulatory role in the DC migration process mediated by CCR7. Mice with DC conditional knock-out lnc-Dpf3 showed an increased DC migration mediated by CCR7, which in turn led to adaptive immuno-over-activeness and increased tissue inflammation. Mechanism studies have found that CCR7 signals inhibit the degradation of RNA mediated by lnc-Dpf3 RNA m6A modification in DC, thereby increasing the lnc-Dpf3 expression. The increased lnc-Dpf3 negative feedback inhibits CCR7-mediated transcription factor HIF-1 alpha activity and glycolysis gene LDHA expression, thereby inhibiting DC's glycolysis level and ultimately negatively regulating CCR7-mediated DC migration.
natural immunity and inflammatory regulation have been the leading research topics in the field of biomedical science. This study reveals a new surface regulatory mechanism for immune inflammation, helps explain the mechanism of inflammatory diseases associated with excessive migration of immune cells, and provides new ideas and targets for the design and exploration of treatment methods for inflammatory diseases. (Source: Science Network Wang Wei)
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