Bacille Calmette-Guérin induces NOD2-dependent nonspecific protection from reinfection via epigenetic reprogramming of monocytes
By J. Kleinnijenhuis, J. Quintin, F. Preijers, L. Joosten, D. Ifrim, Sadia Saeed, C. Jacobs, J. van Loenhout, D. D. de Jong, H. Stunnenberg and 4 more. Proceedings of the National Academy of Sciences of the United States of America, 2012
1,575 citations recorded by the source corpus.
Subfields: Immunology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/c8f0fc48dfb7bc3b451a9943d6f0b17cb259e03b
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Citations in the corpus
- Microglial M1/M2 polarization and metabolic states (2016, background): “, 2011) and a lymphocyte-independent shaping of innate immunity has been termed ‘memory’ (Kurtz and Franz, 2003; Kleinnijenhuis et al., 2012).”
- β-Glucan Reverses the Epigenetic State of LPS-Induced Immunological Tolerance (2016, neutral): “…immunity can have beneficial effects through priming of macrophages for stronger responses to subsequent infection and can be induced by a variety of MAMPs, such as C. albicans (Quintin et al., 2012), Bacille CalmetteGueérin (BCG) vaccine (Kleinnijenhuis et al., 2012), and BG (Saeed et al., 2014).”
- NOD1 and NOD2: signaling, host defense, and inflammatory disease. (2014, background): “Indeed, monocytes can be functionally reprogrammed to exhibit enhanced and lasting protective functions not only against tuberculosis but also against secondary nonmycobacterial challenges through a NOD2-dependent mechanism (Kleinnijenhuis et al., 2012).”
- Glutaminolysis and Fumarate Accumulation Integrate Immunometabolic and Epigenetic Programs in Trained Immunity (2016, background): “…few years, when several studies demonstrated that epige- netic reprogramming forms the basis of innate immune memory in both plants (Muthamilarasan and Prasad, 2013; Shah et al., 2014) and mammals (Kleinnijenhuis et al., 2012; O’Sullivan et al., 2015; Quintin et al., 2012; Saeed et al., 2014).”
- BCG Vaccination Protects against Experimental Viral Infection in Humans through the Induction of Cytokines Associated with Trained Immunity. (2018, methodology): “Using the previously described in vitro model of trained immunity (Bekkering et al., 2016; Kleinnijenhuis et al., 2012), priming of monocytes with IL-1b (1–10 ng/mL) for 24 hr (Figure 6C) enhanced production of the pro-inflammatory cytokines IL-6 and TNFa upon LPS restimula-”
- Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018, neutral): “We have previously reported that brief exposure to oxLDL or BCG also induces trained immunity (Bekkering et al., 2014; Kleinnijenhuis et al., 2012).”
- Immunosenescence and Inflamm-Aging As Two Sides of the Same Coin: Friends or Foes? (2018, background): “One of the most important observations of these last years, besides the discovery of PRR, is the fact that the innate immune system possesses some sort of memory which has been termed trained innate immune memory (22, 23).”
- Oxidized Low-Density Lipoprotein Induces Long-Term Proinflammatory Cytokine Production and Foam Cell Formation via Epigenetic Reprogramming of Monocytes (2014, background): “of proinflammatory cytokines ex vivo after re-exposure to various unrelated pathogens.(13) This enhanced proinflammatory state of the monocytes could be detected ≤1 year after first exposure.”
- Trained immunity: a program of innate immune memory in health and disease (2016, methodology): “BCG vaccination has also been shown to result in an increase in inflammatory mediators produced by monocytes from healthy volunteers, which correlated with parallel changes in a histone modification associated with gene activation (37).”
- mTOR- and HIF-1α–mediated aerobic glycolysis as metabolic basis for trained immunity (2014, background): “In line with the proposal that there are nonspecific adaptive responses in the innate immune system, T and B cell–independent protective effects of monocytes and natural killer (NK) cells have been demonstrated in models of bacterial and viral infections, respectively (5, 6).”