Jennifer Yunyan Zhang
Duke University, NC·Microbiology & Immunology
Skin and tumors both depend on conversations between tissue cells and the immune cells that move in among them. The research described here looks at how molecular signals control those conversations, in two settings: chronic skin inflammation such as psoriasis, and the immune response to tumors after radiation therapy.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Biology
- Topics
K63 ubiquitination
keratinocytes
psoriasis
- Grants
- 2 known grants, through May 2031
What they work on
- Test whether UBE2N's enzyme activity and its partner UBE2V1 maintain normal epidermis and skin immune balance, using conditional genetic mouse models, single-cell transcriptomics and proteomics.
- Determine how much IL1 signaling drives the psoriasis-like inflammation that develops when UBE2N is removed from mouse keratinocytes, the main cells of the outer skin.
- Assess whether drugs that block the receptor for CXCL1/2, signals that attract neutrophils, can reduce neutrophilic dermatosis in mouse models.
- Define how PCSK9, a cholesterol-regulating protein that lowers tumor MHC class I, shapes tumor growth and immune cells after radiotherapy, using transplanted and genetically induced mouse tumors.
- Determine how PCSK9 interacts with the cGAS-STING DNA-sensing pathway after radiation, focusing on STK11/LKB1-mutant tumors, where this pathway is suppressed.
- Test whether the approved PCSK9 inhibitor evolocumab improves radiotherapy and immune checkpoint blockade against irradiated and distant tumors in mice.
More about the research
In both cases the goal is to find specific signals that could be blocked with drugs.
Why it matters
People with psoriasis and neutrophilic skin diseases need better-targeted treatments. This work may identify IL1 signaling and CXCL1/2 receptors as drug targets for some patients. For cancer patients, PCSK9 inhibitors are already approved to lower cholesterol, so if they boost tumor immunity they could move quickly into clinical trials that combine them with radiotherapy and immunotherapy, including for lung tumors with STK11/LKB1 mutations.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Alexander Stegh
Washington University in St Louis, MO·Pharmacology
Determine the cellular, epigenomic, and metabolic mechanisms by which wild-type IDH1 keeps tumor-associated myeloid cells immunosuppressive, using mice in which the enzyme is switched on or deleted only in myeloid cells via tamoxifen-induced LysM-creERT2 recombination.
David Tweardy
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Determine whether the STAT3 inhibitor TTI-101, alone or combined with anti-PD-1 antibody, treats lung tumors effectively in the K-ras mutant CC-LR mouse model of non-small cell lung cancer.
Weili Miao
Stanford University, CA·Biology·Early-career
Define how glucose enables the RNA-binding protein DDX50 to form a complex with RNA and the protein STAU1, and how glucose controls this complex's role in keratinocyte differentiation.
The school
Duke University: 61 labs on PI Pages, $1.6B a year on research, 417 research doctorates a year.
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