Alarmin S100A11 initiates a chemokine response to the human pathogen Toxoplasma gondii.
Alexandra SafronovaAlessandra AraujoEllie T CamanzoTaylor J MoonMichael R ElliottDaniel P BeitingFelix YarovinskyPublished in: Nature immunology (2018)
Toxoplasma gondii is a common protozoan parasite that infects up to one third of the world's population. Notably, very little is known about innate immune sensing mechanisms for this obligate intracellular parasite by human cells. Here, by applying an unbiased biochemical screening approach, we show that human monocytes recognized the presence of T. gondii infection by detecting the alarmin S100A11 protein, which is released from parasite-infected cells via caspase-1-dependent mechanisms. S100A11 induced a potent chemokine response to T. gondii by engaging its receptor RAGE, and regulated monocyte recruitment in vivo by inducing expression of the chemokine CCL2. Our experiments reveal a sensing system for T. gondii by human cells that is based on the detection of infection-mediated release of S100A11 and RAGE-dependent induction of CCL2, a crucial chemokine required for host resistance to the parasite.
Keyphrases
- toxoplasma gondii
- endothelial cells
- induced apoptosis
- innate immune
- high glucose
- dendritic cells
- liver injury
- induced pluripotent stem cells
- drug induced
- binding protein
- poor prognosis
- peripheral blood
- endoplasmic reticulum stress
- liver fibrosis
- signaling pathway
- oxidative stress
- cell cycle arrest
- amino acid
- protein protein
- candida albicans
- dna methylation
- immune response
- long non coding rna
- reactive oxygen species