Supplementary Figure 7: TLR3-mTORC2 axis is required for protection against HSV-1 infection. | Nature Immunology

Supplementary Figure 7: TLR3-mTORC2 axis is required for protection against HSV-1 infection.

From: Combating herpesvirus encephalitis by potentiating a TLR3–mTORC2 axis

Supplementary Figure 7

Prior to its activation, TLR3 is associated with the GTPase Rab7a and is localized in late endosomes/lysosomes around the nucleus. Upon Herpes Simplex Virus-1 (HSV-1) infection, TLR3 is activated and recruits mTORC2, leading to TRAF6-dependent NF-κB activation to produce proinflammatory cytokines such as the chemokine CCL5. TLR3-dependent mTORC2 activation also induces microtubule elongation to the cell periphery by activating PKCs. Rab7a links TLR3-containing lysosomes with elongated microtubules for TLR3 trafficking to the cell periphery. This trafficking is required for the interaction between TLR3 and type I interferon (type I IFN) signaling molecules, such as TRAF3 and mTORC1. A monoclonal antibody to TLR3 shows the rescuing effect against Herpes Simplex Encephalitis by enhancing TLR3 responses. N, nucleus

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