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. Author manuscript; available in PMC: 2015 May 6.
Published in final edited form as: Cell Metab. 2014 May 6;19(5):737–739. doi: 10.1016/j.cmet.2014.04.012

Figure 1.

Figure 1

TLR-mediated reprogramming of cellular metabolism is a requirement for DC effector functions.

TLR signaling via the kinases Tbk1-IKKε and Aktrapidly increases glycolysis by promoting juxtaposition of the rate-limiting glycolytic enzyme HK-II to the outer mitochondrial membrane. Upon translocation,HK-II gains direct access to high concentrations of ATP, which enhances its enzymatic activity. Increased glycolytic flux: a) recharges NADPH through the PPP; b) promotes utilization of citrate and isocitrate for lipogenesis. Together, increased fatty acid synthesis induces ER and Golgi expansion, accommodating cellular demand for the translation, transport and secretion of early activation markers and pro-inflammatory cytokines TNFa and IL-6.