Ryan Nelson
University of Minnesota, MN·Microbiology & Immunology·Early-career
Allergic asthma flares when the lungs encounter an allergen they have met before. Part of this rapid response comes from Th2 tissue-resident memory T cells (Th2-Trm), immune cells that stay near the airways after a first allergic exposure and quickly drive inflammation on re-exposure.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
- Topics
allergic asthma
atopic disease
allergy
- Grants
- 1 known grant, through Dec 2027
What they work on
- Define how allergen-specific regulatory T cells that stay in the lung suppress Th2 resident memory T cells, characterizing their location, persistence, suppressive strength and gene expression in a house dust mite mouse model of asthma.
- Test whether the chemokine receptors CXCR6 and CCR8, homing signals that guide immune cells, position lung-resident Tregs next to Th2 memory cells and support their suppressive function.
- Identify additional genes needed for Tregs to remain resident in the lung, using an in vivo CRISPR-Cas9 screen in house dust mite-specific T cells from allergen-exposed mouse lungs.
More about the research
Regulatory T cells (Tregs), immune cells marked by the protein FoxP3 that calm other immune responses, can suppress allergic inflammation. How they keep the resident memory cells in check is not well understood.
Why it matters
Asthma and other allergic diseases flare when the airways meet allergens they remember. Defining how lung-resident regulatory T cells hold back allergy-driving memory cells, and which homing receptors place them there, could point to new and effective therapies for allergic asthma and other atopic diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Debajyoti Ghosh
University of Cincinnati, OH·Microbiology & Immunology
Determine whether perinatal dysbiosis, an imbalanced microbial community in early life, makes mice more susceptible to skin-associated allergic diseases by weakening the skin barrier.
Robert Winchester
Columbia University, NY·Microbiology & Immunology
Test whether immune checkpoint inhibitors convert PD-1+ tissue-resident memory (TRM) T cells in osteoarthritic joints into inflammatory effector T cells, using a longitudinal patient study that traces T-cell receptor (TCR) clonotypes as lineage barcodes.
Lee Quinton
University of Massachusetts Chan Medical School, MA·Microbiology & Immunology
Map when and where CD4+ resident memory T cells, immune cells that stay in previously infected lungs, become activated near airways and veins while neutrophils spread through the lung, using imaging and cytometry in mouse pneumonia.
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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