Eric Ubil
University of Kentucky, KY·Microbiology & Immunology
Chemotherapy kills tumor cells in a way that can alert the immune system, releasing danger signals that should spark inflammation and an attack on the cancer. Yet many tumors escape this response, and drugs that release the brakes on the adaptive immune system (checkpoint inhibitors such as anti-PD-1) help only some patients.
- Fields
Microbiology & Immunology
Pharmacology
Medicine & Clinical Research
- Topics
cancer immunology
tumor immunology
innate immune checkpoint
- Grants
- 1 known grant, through Jun 2027
What they work on
- Determine how tumor cells regulate secretion of proteins that activate the macrophage Mer receptor, and test whether their levels in human tumors predict response to chemotherapy.
- Identify which chemotherapy drugs produce the strongest immune activation when combined with a PTP1b inhibitor, which blocks the Mer–Stat1–PTP1b complex that lowers MyD88, in mouse tumor models.
- Test how combining chemotherapy with PTP1b inhibition changes the adaptive immune response, including T-cell activity and responsiveness to checkpoint blockade drugs such as anti-PD-1.
More about the research
This project studies a hidden brake on the innate immune system, the body's fast, first-line defense, that tumors use to silence the immune response during chemotherapy.
Why it matters
Many cancer patients do not respond to checkpoint inhibitors or relapse after treatment. Pairing chemotherapy with a PTP1b inhibitor could restore the immune attack that chemotherapy normally triggers. This may offer a new combination therapy for cancers such as melanoma, lung, pancreatic and breast cancer. Measuring Mer-activating proteins in tumors could also help predict which patients will respond to chemotherapy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jun Wang
New York University, NY·Microbiology & Immunology
Determine whether Siglec-15, a tumor-associated immune brake, also suppresses myeloid cells such as macrophages, and identify the receptors it binds on myeloid cells and T cells.
Isabelle Lemasson
East Carolina University, NC·Microbiology & Immunology
Characterize how abnormally high vascular cell adhesion molecule 1, a surface protein that grips neighboring cells, combined with suppressed annexin A1 on HTLV-1-infected T cells, affects transmission of the virus to target CD4+ T cells.
Drew Pardoll
Johns Hopkins University, MD·Microbiology & Immunology
Identify molecules made by regulatory T cells (Tregs), immune cells that suppress other immune cells, that are found specifically in tumors of patients who do not respond to anti-PD-1 or anti-PD-L1 therapy.
The school
University of Kentucky: 34 labs on PI Pages, $528M a year on research, 319 research doctorates a year.
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