The Vaccine Adjuvant Monophosphoryl Lipid A as a TRIF-Biased Agonist of TLR4

By V. Mata‐Haro, C. Cekic, Michael H. Martin, P. Chilton, Carolyn R. Casella, T. Mitchell. Science, 2007

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Macrophage activation by endogenous danger signals (2008, background): “Binding of Lipid IVa to MD-2–TLR4 complex inhibits signalling events mediated by MyD88 and TRIF [30].”
Applications of nanotechnology for immunology (2013, background): “This 'TRIF bias' has been described for particular TLR4 agonists such as MPL 119 , which is an LPS derivative that is used as an adjuvant in numerous vaccines, including licensed recombinant HPV bivalent vaccine 120 .”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “However, the TLR4 agonist monophosphoryl lipid A exhibits low toxicity compared to LPS and possess only weak ability to induce proinflammatory cytokines, which may be explained by its selective activation of the TRAM-TRIF pathway as opposed to the Mal-MyD88 pathway (235).”
Immunological mechanisms of vaccination (2011, background): “Although both lipopolysaccharide and MPL signal via TLR4, the latter signals mainly via TRI”
Vaccine Adjuvants: Putting Innate Immunity to Work (2010, background): “…MPL are recognized specifically by TLR4, but MPL leads to signaling only through the TRIF adaptor, whereas LPS leads to TLR4 activation through both the TRIF and MyD88 pathways (Mata-Haro et al., 2007), the latter pathway resulting in high levels of many inflammatory cytokines, prominently TNF-a.”