Weill Cornell Medicine faculty member Dr. Anna Nam and postdoctoral fellow Dr. Maria Cecilia Lira have been chosen to join the 2025 class of Pew scholars and fellows.

Weill Cornell Medicine researchers have discovered that PD-1—a molecule best known for putting the brakes on immune cells—also plays a critical role in helping T cells become long-term immune defenders in the skin. Early during infection, PD-1 acts like a steering wheel, guiding T cells to become protective resident memory T cells (TRM) that stay in place. These cells remember invading germs or cancer and quickly mount a response if that enemy reappears.

A protein called PAR1 helps lymphatic vessels structurally transform to boost fluid drainage and support healing when the lungs are injured according to researchers from Weill Cornell Medicine. Injury—whether by infection, toxins, or trauma—can cause fluid buildup in the lungs, making it hard to breathe. In response, the body’s lymphatic system, a network of vessels, tissues and organs, ramps up to clear inflammation. Excess fluid called lymph is removed from the body's tissues and returned to the blood for disposal. But the underlying mechanism of this process was unknown.

While glucose, or sugar, is a well-known fuel for the brain, Weill Cornell Medicine researchers have demonstrated that electrical activity in synapses—the junctions between neurons where communication occurs—can lead to the use of lipid or fat droplets as an energy source.

A pretreatment step could help transplanted pancreatic islets survive longer in patients with type 1 diabetes, according to a new preclinical study from Weill Cornell Medicine investigators. One combination of small molecules extended the cells’ lives in female mice, and adding two molecules to the mixture boosted cell survival in male mice.

The findings, published on June 24 in Cell Stem Cell, could allow physicians to treat more patients with fewer cells.

A rare gene mutation that delays Alzheimer’s disease does so by damping inflammatory signaling in brain-resident immune cells, according to a preclinical study led by investigators at Weill Cornell Medicine. The finding adds to growing evidence that brain inflammation is a major driver of neurodegenerative disorders such as Alzheimer’s—and that it may be a key therapeutic target for these disorders.

Thousands of bacterial and other microbial species live in the human gut, supporting healthy digestion, immunity, metabolism and other functions. Precisely how these microbes are protected from immune attack has been unclear, but now a study led by Weill Cornell Medicine investigators has found that this immune “tolerance” to gut microbes depends on an ancient bacterial-sensing protein called STING—normally considered a trigger for inflammation. The surprising result could lead to new treatments for inflammatory bowel disease and other conditions involving gut inflammation.

Using an algorithm they call the Krakencoder, researchers at Weill Cornell Medicine are a step closer to unraveling how the brain’s wiring supports the way we think and act. The study, published June 5 in Nature Methods, used imaging data from the Human Connectome Project to align neural activity with its underlying circuitry.