Inflammatory signals in dendritic cell activation and the induction of adaptive immunity

By O. Joffre, M. Nolte, R. Spörri, C. Reis e Sousa. Immunological Reviews, 2009

607 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a984b7531c24adc70418059f1a191788bb905b10

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In Immunology

Citations in the corpus

TLR-driven early glycolytic reprogramming via the kinases TBK1-IKKε supports the anabolic demands of dendritic cell activation (2014, methodology): “(d) 13C-labeled metabolites in GM-DCs incubated for 1 h with medium (−) or LPS in the presence of 1,2-13C-glucose, detected by NMR spectrometry and presented relative to the total pool of that metabolite (m+1, m+2, m+3 (horizontal axes), mass of metabolite (m) + mass units (1, 2, 3) derived from inc”
AS04, an Aluminum Salt- and TLR4 Agonist-Based Adjuvant System, Induces a Transient Localized Innate Immune Response Leading to Enhanced Adaptive Immunity1 (2009, background): “DCs and monocytes, once activated at the site of injection by the local innate response, can migrate to the draining lymph node to provide essential information, including the antigenic determinants, to T and B cells for the generation of an adaptive response (26, 27).”
The Role of TLR2 in Infection and Immunity (2012, background): “Type I IFN, mainly produced by dendritic cells, can prime natural killer (NK) cells, essential for early infection control (Szomolanyi-Tsuda et al., 2006), and induce maturation of T helper 1 (Th1) cells (Joffre et al., 2009).”
Mitochondria in the regulation of innate and adaptive immunity (2015, positive): “This process, termed DC maturation, also promotes migration of DCs to the T cell zones of the secondary immune organs and is required for proper activation and control of an adaptive immune response (Joffre et al., 2009).”