Tracey Lamb
University of Utah, UT·Microbiology & Immunology
Malaria kills about half a million people a year. Much of the damage comes from the body's own immune response rather than from the parasite directly.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
- Topics
malaria
Plasmodium berghei
acute lung injury
- Grants
- 3 known grants, through Jun 2027
What they work on
- Show whether low-affinity CD8 T cells, whose receptors bind parasite targets weakly, cause experimental cerebral malaria in mice infected with Plasmodium.
- Compare low- and high-affinity CD8 T cells that enter the central nervous system, including how each affects brain microvascular endothelial cells that present parasite antigens.
- Test whether the way Plasmodium antigens are recognized explains why low-affinity CD8 T cells make up most of the anti-parasite response.
- Measure the strength of signal, including 2D affinity and bond lifetime under force, at the receptors of iNKT cell subsets in naive mice and mice infected with P. berghei ANKA.
- Test whether iNKT2-inducing lipid antigens block the expansion and trafficking of IFN-γ-producing CD8 T cells and protect mice from cerebral malaria.
- Determine whether influenza A/X31 co-infection suppresses harmful Plasmodium-reactive CD8 T cells directly or indirectly in mice infected with P. berghei NK65e.
- Test whether arginase 1-producing monocytes recruited by influenza protect mice from malaria-associated lung vascular leak.
More about the research
CD8 T cells, immune cells that normally kill infected cells, drive the brain swelling of cerebral malaria and the lung leakage seen in severe adult malaria. Lamb's research asks what makes these T cells harmful and how they could be held back. The work focuses on three areas: how strongly T cells bind parasite targets, how fast-acting innate immune cells set up the T cell response, and how a second infection can unexpectedly protect the lungs. All three projects use mouse models of Plasmodium, the parasite that causes malaria.
Why it matters
Malaria kills roughly half a million people each year. Severe forms such as cerebral malaria, and the lung vessel leakage seen in adults infected with Plasmodium vivax and P. knowlesi, are driven by T cells. By identifying which T cells cause damage and what restrains them, this work could point to add-on therapies alongside antiparasite drugs. One example is lipids that steer iNKT cells or the Arg1 monocyte pathway. It could also inform future vaccine design.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Patrick Belvitch
University of Illinois Chicago, IL·Medicine & Clinical Research
Determine how CARMIL1, a regulator of actin filament growth, shapes edge actin structures in lung endothelial cells, using biochemistry and advanced imaging after silencing CARMIL1 or overexpressing normal or variant forms.
Geoffrey Hart
University of Minnesota, MN·Microbiology & Immunology
Test whether human NK cells, immune cells that kill antibody-coated targets, clear blood-stage Plasmodium in vivo by transferring them with human anti-merozoite antibodies into immunodeficient mice.
Yasuhiro Suzuki
University of Kentucky, KY·Microbiology & Immunology
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.
The school
University of Utah: 58 labs on PI Pages, $789M a year on research, 366 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.