Journal
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2019.00061
Keywords
apicomplexa; CNS infection; dendritic cell; microglia; motility; GABA receptor
Categories
Funding
- Swedish Research Council [2018-02411]
- Fredrik and Ingrid Thurings Foundation [2017-00349, 2018-00404]
- Olle Engkvist Foundation [193-609]
- Swedish Research Council [2018-02411] Funding Source: Swedish Research Council
Ask authors/readers for more resources
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 gamma-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 ismediated 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 andmicroglia. 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available