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Dendritic cells (DCs) are regarded as the gatekeepers of the immune system but can also mediate systemic dissemination of the obligate intracellular parasite  Toxoplasma gondii . Here, we review the current knowledge on how  T. gondii  hijacks the migratory machinery of DCs and microglia. Shortly after active invasion by the parasite, infected cells synthesize and secrete the neurotransmitter γ-aminobutyric acid (GABA) and activate GABA-A receptors, which sets on a hypermigratory phenotype in parasitized DCs  in vitro  and  in vivo . The signaling molecule calcium plays a central role for this migratory activation as signal transduction following GABAergic activation is mediated via the L-type voltage-dependent calcium channel (L-VDCC) subtype Ca v 1.3. These studies have revealed that DCs possess a GABA/L-VDCC/Ca v 1.3 motogenic signaling axis that triggers migratory activation upon  T. gondii  infection. Moreover, GABAergic migration can cooperate with chemotactic responses. Additionally, the parasite-derived protein Tg14-3-3 has been associated with hypermigration of DCs and microglia. We discuss the interference of  T. gondii  infection with host cell signaling pathways that regulate migration. Altogether,  T. gondii  hijacks non-canonical signaling pathways in infected immune cells to modulate their migratory properties, and thereby promote its own dissemination.

frontiers in cellular and infection microbiology

Calling in the CaValry—Toxoplasma gondii Hijacks GABAergic Signaling and Voltage-Dependent Calcium Channel Signaling for Trojan horse-Mediated Dissemination