首页|LNCGM1082-mediated NLRC4 activation drives resistance to bacterial infection
LNCGM1082-mediated NLRC4 activation drives resistance to bacterial infection
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The activation of NLRC4 is a major host response against intracellular bacteria infection.However,NLRC4 activation after a host senses diverse stimuli is difficult to understand.Here,we found that the lncRNA LNCGM1082 plays a critical role in the activation of NLRC4.LNCGM1082 in macrophages affects the maturation of interleukin(IL)-1β and pyroptotic cell death only after exposure to an NLRC4 ligand.Similar to NLRC4-/-mice,LNCGM1082-/-mice were highly sensitive to Salmonella Typhimurium(S.T)infection.LNCGM1082 deficiency in mouse or human macrophages inhibited IL-1β maturation and pyroptosis.Mechanistically,LNCGM1082 induced the binding of PKCδ with NLRC4 in both mice and humans.In contrast,NLRC4 did not bind PKCδ in LNCGM1082-/-macrophages.The activity of the lncRNA LNCGM1082 induced by S.T may be mediated through TLR5 in the macrophages of both mice and humans.In summary,our data indicate that TLR5-mediated LNCGM1082 activity can promote the binding of PKCδ with NLRC4 to activate NLRC4 and induce resistance to bacterial infection.
Department of Immunology,Nankai University School of Medicine and Translational Medicine Institute,Affiliated Tianjin Union Medical Center of Nankai University,Nankai University,Tianjin 300071,China
State Key Laboratory of Medicinal Chemical Biology,Nankai University,Tianjin 300071,China
College of Life Science,Nankai University,Tianjin 300121,China
China National Center for Bioinformation&Beijing Institute of Genomics,Chinese Academy of Sciences,Beijing,China
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NSFCNSFCNSFCNSFCNSFCTianjin Science and Technology CommissionA Ministry of Science and TechnologyState Key Laboratory of Medicinal Chemical BiologyFundamental Research Funds for the Central University,Nankai university
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