Susheela Tridandapani
Ohio State University, OH·Microbiology & Immunology
Antibody drugs fight cancer partly by flagging tumor cells for destruction by the patient's own immune cells. Monocytes and macrophages — white blood cells that engulf and clear flagged targets — are central to that process.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Pharmacology
- Topics
chronic lymphocytic leukemia
mifamurtide
Fc gamma receptor
- Grants
- 1 known grant, through Aug 2029
What they work on
- Determine how stimulating NOD2, an intracellular bacterial-fragment sensor, reshapes monocytes and CLL nurse-like macrophages, including loss of the inhibitory phosphatase SHIP1 and receptor CD31 and gain of the activating Fc receptor FcγRI.
- Examine how NOD2 stimulation of monocytes influences natural killer cells, testing whether the effect requires cell-to-cell contact or soluble cytokines and how it changes NK cell maturation and cytotoxicity.
- Test in vivo whether treatment with a NOD2 agonist such as MTP-PE (mifamurtide) produces the predicted changes in monocytes, nurse-like cells and NK cells and yields stronger antitumor activity.
- Link NOD2-driven changes in Fcγ receptor signaling to improved antibody-mediated depletion of chronic lymphocytic leukemia cells, building on CD20 antibody regimens used with the BTK inhibitor acalabrutinib.
More about the research
In chronic lymphocytic leukemia (CLL), a common blood cancer of B cells, these cells are held in a suppressed state. Worse, unusually large macrophages in CLL patients, known as nurse-like cells, actively help leukemia cells survive and multiply. The long-term goal here is to understand the receptors these cells use to grab antibodies, called Fc gamma receptors, and to use that knowledge to make antibody therapies work better.
Why it matters
CLL patients benefit from CD20-targeting antibodies, but suppressed monocytes and macrophages limit how well those antibodies clear leukemia cells. By defining how NOD2 activation reverses that suppression, this work aims to justify clinical testing of mifamurtide — a drug with an existing safety record — as an add-on to improve antibody therapy for chronic lymphocytic leukemia.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Randall Davis
University of Alabama at Birmingham, AL·Microbiology & Immunology
Determine how FCRL1, a B cell surface receptor overproduced in leukemia, influences B cell responses in human and mouse disease models of chronic lymphocytic leukemia and immune tolerance.
Geoffrey Hart
University of Minnesota, MN·Microbiology & Immunology
Test whether human NK cells, immune cells that kill antibody-coated targets, clear blood-stage Plasmodium in vivo by transferring them with human anti-merozoite antibodies into immunodeficient mice.
Wayne Yokoyama
Washington University in St Louis, MO·Microbiology & Immunology
Identify the effector mechanisms by which NK cells constrain immune checkpoint therapy in mouse tumor models, using NK cell depletion, NK-deficient mice and transfer of NK cells into tumors.
The school
Ohio State University: 71 labs on PI Pages, $1.6B a year on research, 882 research doctorates a year.
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