Jennifer Oyler-Yaniv, 2026
Who she is
Jen Oyler-Yaniv received her BS from Saint Joseph’s University in 2005, majoring in Biology and minoring in Philosophy. She then went on to earn a PhD in Immunology from Weill Cornell in 2016, where she focused on the spatial and temporal control of cytokine propagation and persistence during healthy immune responses, and in cancer. She performed postdoctoral studies at UCLA, where she used microscopy to investigate how cytokines affect a tissues’ tolerance for damage in order to restrict the spread of viruses. In 2021, she and her partner Alon Oyler-Yaniv jointly opened their lab together in the Department of Systems Biology.
What she does
The immune system is unlike other organ systems in that it is comprised of cells that are constantly on the move, patrolling the body for viruses, bacteria, and even cancer cells. When a threat is sensed, immune cells become activated and emit warning signals and cues that recruit other immune cells and tailor the immune response to the threat. These signals – chemokines and cytokines – cause immune cells to spatially re-organize into a temporary micro-organ or niche. In this close-knit environment, the cells interact and specialize to more effectively fight the pathogen. Despite the importance of cytokines to enable the immune system to function properly, they can damage healthy tissues and contribute to many different human diseases. A key factor that controls how potentially dangerous cytokines can be, is the question of how far they can spread away from their source. If they can spread over vast distances – such as to distant organ systems or through an entire tissue, they can potentially harm many cells. However, if they don’t get past a single cell, they might not be able to warn cells that are further away.
Our lab is focused on two major themes relating to cytokine spread. First, we investigate the factors that determine how far cytokines can spread away from their source. We are inspired by the physics that determine how small molecules spread through space and have applied the same math to this biological problem. A major advantage is that our math is generalizable, which gives us flexibility in studying different organs or diseases. Second, we study how cells that assemble into these ‘micro-organs’ change their function and behavior to eliminate threats. In addition to using math models, we use microscopy to visualize how cells re-organize in time and space as they eliminate viruses and cancer.
News from the Lab
Cytokine are small, often secreted proteins that mediate cell communication in the immune system. They recruit and organize immune cells and scale and specify the response. While we know a great deal about them, the spatial extent of spread away from their source of production, and the factors that govern that spread, were unclear. Key barriers to this understanding were the intractability of in vivo models, yet in vitro settings lacked the geometry and density seen in vivo. We also lacked a quantitative and generalizable framework to describe their spread. To overcome these barriers, we engineer ex vivo cultures that mimic in vivo conditions, but afford more experimental control. We hypothesized that cytokine spread could be explained by the biophysics of diffusion and receptor-mediated consumption and used our experimental tools to rigorously test predictions from our model, which validated this hypothesis. We also confirmed that our framework held true in vivo in mice and in human tumors and – most exciting – that natural immune responses tune some of the parameters of the model, which predictably extends or confines spread. Our ongoing work addresses (1) whether our quantitative framework can describe the spread of small immune-transmitters and signaling metabolites within 2-D epithelia, (2) what are the natural length-scales for common T cell derived cytokines in the lymphoid organs, and (3) how do cytokine length-scales evolve and change over time as a result of feedbacks between communicating cells within niches.
