Scott McPherson
University of Minnesota, MN·Microbiology & Immunology
The eye has to stay protected against infection while avoiding inflammation that could damage vision. Inflammatory eye diseases can cause visual impairment or even blindness.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
- Topics
retinal autoimmunity
inflammatory eye disease
ocular immunology
- Grants
- 1 known grant, through Dec 2026
What they work on
- Define how retinal microglia, especially the subset that acts as dendritic cells, present retinal self-antigens to T cells and drive autoimmune disease, using R161H mice with transgenic tracking and depletion of dendritic cells and microglia.
- Distinguish the roles of resident retinal microglia and non-immune retinal cells in turning CD4+ T cells into regulatory T cells (Tregs) or unresponsive anergic T cells inside the retina.
- Test whether the retina continually generates self-antigen-specific Tregs 'on demand', using transgenic mice that allow Tregs to be tracked and depleted in the R161H model of spontaneous retinal autoimmunity.
- Test local therapies that alter retinal microglia or other antigen-presenting cells to limit T cell costimulation and promote anergic T cells and Tregs, reducing inflammatory injury to the retina.
More about the research
Keeping this balance depends on T cells, white blood cells that come in several kinds. Effector T cells attack targets. Regulatory T cells (Tregs) calm immune responses. Anergic T cells have been switched into an unresponsive, non-dividing state. When Tregs are missing, T cells that recognize the body's own proteins (self-antigens) can attack tissues, including the retina, the light-sensing layer at the back of the eye. This project asks how the retina itself keeps these T cells in check.
Why it matters
Inflammatory diseases of the eye threaten vision and can lead to blindness. By clarifying how the retina locally restrains self-reactive T cells, this work could point to local treatments that tune antigen-presenting cells inside the eye. Such treatments could boost protective regulatory and anergic T cells and limit inflammatory damage, which may benefit patients with inflammatory eye disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
James Walsh
Washington University in St Louis, MO·Microbiology & Immunology·Early-career
Test whether retinal antigens activate the adaptive immune system within the choroid, the immune-rich layer behind the retina, and whether this drives autoimmune uveitis in experimental models.
Hussein Sultan
Washington University in St Louis, MO·Microbiology & Immunology
Determine how the EBI3 subunit of the suppressive cytokine IL-35 drives induction of Tr1 regulatory CD4 T cells, using IL-35 reporter mice in established tumor models to identify which cells produce it.
Peter Aidan Savage
University of Chicago, IL·Microbiology & Immunology
Define the biophysical and structural basis by which T cell receptors from regulatory and conventional CD4+ T cells recognize the same self-peptide displayed on MHC class II, testing whether a more centered binding mode increases signaling sensitivity.
The school
University of Minnesota: 88 labs on PI Pages, $1.4B a year on research, 722 research doctorates a year.
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