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CircPRKD3-loaded exosomes concomitantly elicit tumor growth inhibition and glioblastoma microenvironment remodeling via inhibiting STAT3 signaling.
Neuro Oncol
January 2025
Department of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, P.R. China.
Background: Glioblastoma stem cells (GSCs) and their exosomes (exos) are involved in shaping the immune microenvironment, which is important for tumor invasion and recurrence. However, studies involving GSC-derived exosomal circular RNAs (GDE-circRNAs) in regulating tumor microenvironment (TME) remain unknown. Here, we comprehensively evaluated the significance of a novel immune-related GDE-circRNA in glioma microenvironment.
View Article and Find Full Text PDFAPOBEC-1 cofactors regulate APOBEC3-induced mutations in hepatitis B virus.
J Virol
January 2025
Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA.
Unlabelled: APOBEC3 proteins (A3s) play an important role in host innate immunity against viruses and DNA mutations in cancer. A3s-induced mutations in both viral and human DNA genomes vary significantly from non-lethal mutations in viruses to localized hypermutations, such as kataegis in cancer. How A3s are regulated remains largely unknown.
View Article and Find Full Text PDFcoordinates the IL-10 inducing activity of .
Microbiol Spectr
January 2025
Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Unlabelled: The intestine is home to a complex immune system that is engaged in mutualistic interactions with the microbiome that maintain intestinal homeostasis. A variety of immune-derived anti-inflammatory mediators have been uncovered and shown to be critical for maintaining these beneficial immune-microbiome relationships. Notably, the gut microbiome actively invokes the induction of anti-inflammatory pathways that limit the development of microbiome-targeted inflammatory immune responses.
View Article and Find Full Text PDFCD20 and CD19 promote proliferation driven by the IgM-TLR9-L265P MyD88 complex.
Int Immunol
January 2025
Division of Innate Immunity, The Institute of Medical Science, The University of Tokyo; Minato-ku, Tokyo 108-8639, Japan.
The cancer driver mutation L265P MyD88 is found in approximately 30 % of cases in the activated B cell-like subgroup of diffuse large B cell-like lymphoma (ABC DLBCL). L265P MyD88 forms a complex with TLR9 and IgM, referred to as the My-T-BCR complex, to drive proliferation. We here show that the B cell surface molecules CD19 and CD20 enhance proliferation mediated by the My-T-BCR complex.
View Article and Find Full Text PDFTLR7 responses in glomerular macrophages accelerate the progression of glomerulonephritis in NZBWF1 mice.
Int Immunol
January 2025
Division of Innate Immunity, The Institute of Medical Science, The University of Tokyo; Minato-ku, Tokyo 108-8639, Japan.
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the production of autoantibodies and damage to multiple organs. Glomerulonephritis, a manifestation involving glomerular deposition of immune complexes and complement components, significantly contributes to disease morbidity. Although the endosomal single-stranded RNA sensor TLR7 is known to drive glomerulonephritis by promoting autoantibody production in B cells, the contribution of macrophage TLR7 responses to glomerulonephritis remains poorly understood.
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