Yasuhiro Suzuki
University of Kentucky, KY·Microbiology & Immunology
Toxoplasma gondii is a single-celled parasite that can hide in the brain for life as a chronic infection. If the immune system weakens, as in people with AIDS, the parasite can reactivate and multiply as its fast-growing tachyzoite form.
- Fields
Microbiology & Immunology
Neuroscience
Medicine & Clinical Research
- Topics
Toxoplasma gondii
toxoplasmosis
toxoplasmic encephalitis
- Grants
- 2 known grants, through Jul 2029
What they work on
- Test whether interferon-gamma (IFN-γ) made by microglia, the brain's resident immune cells, recruits monocytes, NK cells and ILC1 cells and activates their IFN-γ production to limit Toxoplasma growth, using mice lacking IFN-γ only in microglia.
- Determine whether microglial IFN-γ draws protective CD8+ T cells to brain areas of tachyzoite growth and increases MHC class I antigen presentation there to activate those T cells and prevent toxoplasmic encephalitis.
- Identify Toxoplasma gondii antigens that activate IFN-γ-producing CD8+ T cells capable of preventing encephalitis for each of the human HLA-A2, -A11 and -B7 molecules, using transgenic mice that express these HLA types.
- Determine whether CD180, a microbe-sensing surface molecule on microglia and macrophages, drives IFN-γ and TNF-α production and promptly activates innate and T-cell immunity against reactivating brain Toxoplasma infection.
- Test whether NOD1, an internal sensor of microbial molecules, in microglia and macrophages promotes IFN-γ and TNF-α production and protective immunity that prevents reactivation of cerebral Toxoplasma infection.
More about the research
This causes toxoplasmic encephalitis (TE), a life-threatening brain inflammation. Both projects ask how the brain's own cells detect early parasite growth and call in the immune defenses that keep the infection in check. The work centers on interferon-gamma (IFN-γ), a signaling molecule that switches on anti-parasite defenses. Earlier work from the team found that IFN-γ made by brain-resident cells is crucial for this protection, and that microglia, the brain's resident immune cells, produce IFN-γ when tachyzoites grow.
Why it matters
Toxoplasmic encephalitis is a deadly opportunistic infection in people with AIDS. Identifying the parasite antigens that activate protective CD8+ T cells for common human HLA types could provide a basis for a vaccine. Such a vaccine, given to people co-infected with HIV and Toxoplasma before their CD4 counts drop, might prevent the disease. Knowing how brain sensors and microglia trigger defenses could also reveal general brain mechanisms against infection.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Microglial IFN-y production is a key defense system to coordinate both innate and T cell-mediated protective immunity in the brain for preventing reactivation of cerebral Toxoplasma infection
NIH · Aug 2025 – Jul 2029
Protective roles of CD180 and NOD1 in the protective immunity against cerebral Toxoplasma infection
NIH · Jul 2025 – Jun 2027
Closest labs
Daniel Ram
University of Central Florida, FL·Microbiology & Immunology
Develop a gold nanoparticle platform that displays chosen peptides on HLA-E, a non-classical MHC class I molecule, to replace stressed cell lines as a reproducible and scalable peptide-presentation method.
Tracey Lamb
University of Utah, UT·Microbiology & Immunology
Show whether low-affinity CD8 T cells, whose receptors bind parasite targets weakly, cause experimental cerebral malaria in mice infected with Plasmodium.
William Geisler
University of Alabama at Birmingham, AL·Medicine & Clinical Research·Early-career
Determine whether the HLA-DQB1*06 gene variant and chlamydia-specific CD4+ IFN-gamma responses from helper T cells can predict new Chlamydia trachomatis infections in women, to guide testing frequency.
The school
University of Kentucky: 34 labs on PI Pages, $528M a year on research, 319 research doctorates a year.
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