Schematic illustration.

In un-infected macrophages [1], VCL associates with PIP2 and p85α, preventing activation of downstream Akt phosphorylation and thereby favoring macrophage killing of P. gingivalis when cells are infected. TLR2 senses P. gingivalis and is induced to interact with VCL [2], which causes VCL to dissociate from PIP2 and p85α [3]. This enables PI3K conversion of PIP2 to PIP3, and subsequent phosphorylation of Akt [4], leading to increased intracellular survival. Fig 7 was created with BioRender.com.