Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 15 (12), e1008097

Human Immunity to Toxoplasma Gondii


Human Immunity to Toxoplasma Gondii

Daniel Fisch et al. PLoS Pathog.

Conflict of interest statement

The authors have declared that no competing interests exist.


Fig 1
Fig 1. Systemic and cellular human response to Toxoplasma infection.
Left: Systemic response to Tg-infection: Infected cells and cells that have phagocytosed Tg parasites at a site of infection sense the presence of the pathogen via the indicated PRRs and defence proteins and react by production of proinflammatory cytokines and chemokines like CCL2, IL-1β, and IL-12. This cytokine presence will trigger IFNγ–production by Th1 and NK cells. Right: Cellular response to Tg-infection: IFNγ and potentially other cytokines trigger infected cells to mount a cell-intrinsic defence against the PV. Mechanisms include ubiquitin-driven non-canonical autophagy of the entire PV and growth stunting; marking the PV with Ub, LAMP1, and the autophagy adapter proteins NDP52 and p62, followed by acidification of the vacuoles and killing of the parasite; recruitment of GBP1 to Tg vacuoles to disrupt them and expose the parasite within or growth restriction of Tg by GBP1 without translocation to the vacuole; and host cell death in response to opened PVs and leakage of pathogen-associated molecular patterns into the cytosol for detection by PRRs. The exact mechanisms highly depend on the cell type and the Tg strain infecting the cells. AIM, absent in melanoma 2; ASC, apoptosis-associated speck-like protein containing a CARD; CASP, caspase; CCL, chemokine (C-C motif) ligand; GBP, guanylate binding protein; IL, interleukin; IFNγ, interferon gamma; LAMP, lysosome-associated membrane protein; NDP52, nuclear domain 10 protein 52; NK, natural killer; NLRP, nucleotide-binding oligomerization domain, Leucine rich repeat and Pyrin domain containing; PAMP, pathogen-associated molecular patterns; PRR, pattern recognition receptor; PV, parasitophorous vacuole; Tg, Toxoplasma gondii; Th, T helper cell; TNFα, tumour necrosis factor α; Ub, Ubiquitin.

Similar articles

See all similar articles


    1. Pappas G, Roussos N, Falagas ME. Toxoplasmosis snapshots: Global status of Toxoplasma gondii seroprevalence and implications for pregnancy and congenital toxoplasmosis. Int J Parasitol. 2009. October 1;39[12]:1385–94. 10.1016/j.ijpara.2009.04.003 - DOI - PubMed
    1. Xiao J, Yolken RH. Strain hypothesis of Toxoplasma gondii infection on the outcome of human diseases. Acta Physiol. 2015. April;213[4]:828–45. - PMC - PubMed
    1. Hill D, Dubey JP. Toxoplasma gondii: transmission, diagnosis and prevention. Clin Microbiol Infect. 2002. October 1;8[10]:634–40. 10.1046/j.1469-0691.2002.00485.x - DOI - PubMed
    1. Harker KS, Ueno N, Lodoen MB. Toxoplasma gondii dissemination: a parasite’s journey through the infected host. Parasite Immunol. 2015. March 1;37[3]:141–9. 10.1111/pim.12163 - DOI - PubMed
    1. Gazzinelli RT, Mendonça-Neto R, Lilue J, Howard J, Sher A. Innate resistance against Toxoplasma gondii: An evolutionary tale of mice, cats, and men. Cell Host Microbe. 2014. February 12;15[2]:132–8. 10.1016/j.chom.2014.01.004 - DOI - PMC - PubMed

Publication types