Journal
INTERNATIONAL IMMUNOLOGY
Volume 30, Issue 3, Pages 113-119Publisher
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxy004
Keywords
acquired immunity; cell-autonomous immunity; IFN-inducible GTPases; innate immunity; IFN-gamma
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Funding
- Research Program on Emerging and Re-emerging Infectious Diseases from Agency for Medical Research and Development (AMED) [17fk0108120h0001]
- Japanese Initiative for Progress of Research on Infectious Diseases for Global Epidemics from Agency for Medical Research and Development (AMED) [17fm0208018h0001]
- Ministry of Education, Culture, Sports, Science and Technology [17K15677]
- Cooperative Research Grant of the Institute for Enzyme Research, Joint Usage/Research Center, Tokushima University
- Takeda Science Foundation
- Ohyama Health Foundation
- Heiwa Nakajima Foundation
- Cell Science Research Foundation
- Mochida Memorial Foundation
- Medical and Pharmaceutical Research
- Senri Life Science Research Foundation
- Research Foundation for Microbial Diseases of Osaka University
- Grants-in-Aid for Scientific Research [17K19556, 17K15677, 15H04745] Funding Source: KAKEN
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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-gamma, which robustly stimulates cell-autonomous immunity in cells infected with T. gondii. IFN-gamma-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-gamma-mediated cell-autonomous immunity against T. gondii infection.
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