Collynn Woeller
University of Rochester, NY·Microbiology & Immunology
In thyroid eye disease, the body's own antibodies attack the tissues behind the eye. Those tissues swell and scar, pushing the eyes forward, causing double vision and lid changes, and in severe cases squeezing the optic nerve badly enough to threaten sight.
- Fields
Microbiology & Immunology
Pharmacology
Medicine & Clinical Research
- Topics
thyroid eye disease
thyroid-associated orbitopathy
Graves' disease
- Grants
- 1 known grant, through Jul 2027
What they work on
- Define the molecular steps by which the aryl hydrocarbon receptor, a chemical-sensing transcription factor, blocks activation of orbital fibroblasts — the connective-tissue cells behind the eye that turn into fat cells and scar-forming myofibroblasts in thyroid eye disease.
- Test whether cigarette smoke exposure of orbital fibroblasts boosts hypoxia inducible factor 1 alpha and insulin-like growth factor 1 receptor signaling while suppressing the aryl hydrocarbon receptor, explaining why smoking is a major risk factor.
- Determine whether compounds that activate the aryl hydrocarbon receptor can block the signaling through the thyroid stimulating hormone receptor and IGF1R that patient autoantibodies trigger in orbital fibroblasts.
- Establish how IGF1R and the thyroid stimulating hormone receptor interact in the presence of disease autoantibodies to drive fibroblast proliferation and excess hyaluronan and collagen production.
More about the research
It is the most common disorder of the eye socket and appears in up to half of people with Graves' disease, an autoimmune thyroid condition. There is no cure; steroids, radiation and surgery manage symptoms. This project asks how the disease starts at the level of single cells, with the goal of finding a pathway that can be switched on to stop it.
Why it matters
Thyroid eye disease disfigures and can blind patients, and only one disease-specific drug exists. Showing that the aryl hydrocarbon receptor restrains the signaling that makes orbital fibroblasts expand and scar would identify a druggable target that works by a different route than existing antibody therapy. It would also explain mechanistically why smoking worsens the disease, strengthening the case for smoking cessation in patients with Graves' disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
John Mountz
University of Alabama at Birmingham, AL·Microbiology & Immunology
Determine which IL-4-induced tryptophan metabolic signals block TLR7-driven autoantibody-precursor B cells in vivo, comparing wild-type mice with mice lacking the B-cell enzymes IL4i1 and Ido1 or the metabolite sensor AhR.
Marlies Meisel
University of Pittsburgh, PA·Microbiology & Immunology
Test whether checkpoint-inhibitor-response-associated gut bacteria convert dietary tryptophan into molecules that activate the aryl hydrocarbon receptor (AhR) and strengthen interferon-gamma-producing Tc1 CD8 T cells, in cell culture.
Shelley Tischkau
Southern Illinois University-Carbondale, IL·Physiology
Test whether restricted feeding, limiting food intake to set times of day, can reset circadian clock function and restore adipose tissue rhythms after the clock is disrupted by chronic activation of the aryl hydrocarbon receptor (AhR) by pollutants such as dioxins.
The school
University of Rochester: 38 labs on PI Pages, $492M a year on research, 308 research doctorates a year.
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