TY - JOUR
T1 - Host immune responses to Toxoplasma gondii
AU - Sasai, Miwa
AU - Pradipta, Ariel
AU - Yamamoto, Masahiro
N1 - Funding Information:
Our work was supported by the Research Program on Emerging and Re-emerging Infectious Diseases (17fk0108120h0001) and the Japanese Initiative for Progress of Research on Infectious Diseases for Global Epidemics (17fm0208018h0001) from the Agency for Medical Research and Development (AMED), a Grant-in-Aid for Scientific Research on Innovative Areas (17K15677) from the Ministry of Education, Culture, Sports, Science and Technology, a Cooperative Research Grant of the Institute for Enzyme Research, Joint Usage/Research Center, Tokushima University, the Takeda Science Foundation, the Ohyama Health Foundation, the Heiwa Nakajima Foundation, the Cell Science Research Foundation, the Mochida Memorial Foundation on Medical and Pharmaceutical Research, the Senri Life Science Research Foundation and the Research Foundation for Microbial Diseases of Osaka University.
Publisher Copyright:
© The Japanese Society for Immunology. 2018.
PY - 2018/3/1
Y1 - 2018/3/1
N2 - Toxoplasma gondii can infect homoeothermic animals including humans and cause lethal toxoplasmosis in immunocompromised individuals. When hosts are infected with T. gondii, the cells induce immune responses against T. gondii. The pathogen infection is recognized by immune sensors that directly detect T. gondii structural components, leading to production of pro-inflammatory cytokines and chemokines. Antigen-presenting cells such as macrophages and dendritic cells strongly activate T cells and induce development of T h 1 cells and antigen-specific killer CD8 T cells. These T cells and Group 1 innate lymphoid cells are main producers of IFN-γ, which robustly stimulates cell-autonomous immunity in cells infected with T. gondii. IFN-γ-inducible effectors such as IFN-inducible GTPases, inducible nitric oxide synthase and indoleamine-2,3- dioxygenase differentially play important roles in suppression of T. gondii growth and its direct killing in anti-T. gondii cell-autonomous immune responses. In this review, we will describe our current knowledge of innate, adaptive and IFN-γ-mediated cell-autonomous immunity against T. gondii infection.
AB - Toxoplasma gondii can infect homoeothermic animals including humans and cause lethal toxoplasmosis in immunocompromised individuals. When hosts are infected with T. gondii, the cells induce immune responses against T. gondii. The pathogen infection is recognized by immune sensors that directly detect T. gondii structural components, leading to production of pro-inflammatory cytokines and chemokines. Antigen-presenting cells such as macrophages and dendritic cells strongly activate T cells and induce development of T h 1 cells and antigen-specific killer CD8 T cells. These T cells and Group 1 innate lymphoid cells are main producers of IFN-γ, which robustly stimulates cell-autonomous immunity in cells infected with T. gondii. IFN-γ-inducible effectors such as IFN-inducible GTPases, inducible nitric oxide synthase and indoleamine-2,3- dioxygenase differentially play important roles in suppression of T. gondii growth and its direct killing in anti-T. gondii cell-autonomous immune responses. In this review, we will describe our current knowledge of innate, adaptive and IFN-γ-mediated cell-autonomous immunity against T. gondii infection.
KW - Acquired immunity
KW - Cell-autonomous immunity
KW - IFN-inducible GTPases
KW - IFN-γ
KW - Innate immunity
UR - https://www.scopus.com/pages/publications/85050630727
U2 - 10.1093/intimm/dxy004
DO - 10.1093/intimm/dxy004
M3 - Article
C2 - 29408976
AN - SCOPUS:85050630727
SN - 0953-8178
VL - 30
SP - 113
EP - 119
JO - International Immunology
JF - International Immunology
IS - 3
ER -