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Researchers Identify Gut Cells That Prevent Food Allergies

For millions of Americans, including 4 million children, life-threatening food allergies are a harsh reality. But what if scientists could identify the cells responsible for preventing these reactions? A groundbreaking study by researchers at Washington University School of Medicine in St. Louis has made just that possible.

The study, published online April 3 in Cell and appearing in print May 15, reveals that a specific type of immune cell called RORγt+ dendritic cells plays a crucial role in preventing food allergies. In the absence of these cells, mice experienced gut inflammation and an allergic response to food.

“We are seeing a rapid global increase in food allergies that significantly impact quality of life,” said Marco Colonna, MD, the Robert Rock Belliveau, MD, Professor of Pathology at WashU Medicine. “The lack of therapeutics to prevent and manage food allergies complicates the growing public health issue.”

Colonna’s lab aimed to uncover the players working to establish tolerance to food allergens. They discovered that RORγt+ dendritic cells pick up food particles, chop them into fragments, and present them to the immune system’s T cells, instructing those cells to remain unresponsive to harmless intruders.

The researchers treated mice with ovalbumin, a highly allergenic protein found in egg whites, orally and then intranasally. Mice lacking gut RORγt+ dendritic cells showed signs of allergic lung inflammation, while mice with these cells did not.

“By removing RORγt+ dendritic cells from the gut in mice, we broke tolerance to food allergens,” said Patrick Rodrigues, PhD, a postdoctoral scholar and co-first author. “The discovery is now inspiring us to see if we can do the opposite: prevent food allergies by supporting the activity of this cell population.”

This breakthrough has significant implications for developing preventive treatments for food allergies. The researchers believe that targeting the activity of RORγt+ dendritic cells might work even further upstream to prevent an immune response from first being triggered.

“If that proves to be true, a therapy supporting the activity of this small population of cells might offer lasting tolerance to food allergens,” said Shitong Wu, an MD/PhD student and co-first author.

The dust on Mars poses a significant threat to the health of future astronauts. A recent study, led by researchers from the University of Colorado Boulder and the Keck School of Medicine at the University of Southern California, has taken a comprehensive look at the chemical ingredients that make up Martian dust and their potential impacts on human health.

The study’s findings are alarming. Long-term exposure to Martian dust could lead to chronic respiratory problems, thyroid disease, and other health issues. The researchers drew on data from rovers on Mars and even Martian meteorites to better understand what makes up the planet’s dust.

Their analysis revealed a “laundry list” of chemical compounds that could be dangerous for people when inhaled in large quantities and over long periods of time. These include minerals rich in silicates and iron oxides, metals like beryllium and arsenic, and highly oxidizing compounds called perchlorates.

Perchlorates are particularly concerning, as they can interfere with human thyroid function, leading to severe anemia. Even inhaling a few milligrams of perchlorates in Martian dust could be dangerous for astronauts.

The researchers emphasize that prevention is key. They suggest that astronauts take iodine supplements to boost their thyroid function and that filters specifically designed to screen out Martian dust are essential for keeping the air in living spaces clean.

As humans prepare to set foot on Mars, it’s essential to consider these health risks and take proactive measures to mitigate them. By doing so, we can ensure a safer and healthier journey for our astronauts as they explore the Red Planet.

The autoimmune disease affects millions of people worldwide, where the body mistakenly attacks healthy tissues due to an overactive immune response. Scientists have long understood how false alarms are triggered, but the subsequent step of dispatching the immune response has remained a mystery. Researchers at Washington University School of Medicine and the Perelman School of Medicine at the University of Pennsylvania have now identified a crucial component in launching the immune activity – and its overactivity.

The researchers discovered that ArfGAP2, a protein found in cells, is responsible for spurring the release of infection-fighting molecules. This protein’s role in the immune system was previously unknown, making it a promising target for therapies to prevent overreactive immune responses at the root of several debilitating illnesses. Their study, published online in Cell, highlights the potential for treating autoimmune disorders by controlling the release process.

By studying a rare autoimmune disease called STING-associated vasculopathy with onset in infancy (SAVI), researchers gained insight into how this condition occurs due to changes in the protein STING. This protein acts as a molecular watchdog that responds to viral DNA, activating the cell’s immune proteins and signaling to the body’s immune system where to attack.

The team made a groundbreaking discovery: ArfGAP2 plays a novel role in releasing immune response proteins from cells, which was previously unknown. In addition, they validated this finding by testing it in SAVI cells that did not produce ArfGAP2. Without this protein, STING could not drive the release of immune proteins.

“This is like a train station and ArfGAP2 is acting as the conductor, directing which molecules are to be shipped out,” said David Kast, an assistant professor at WashU Medicine. “If STING and ArfGAP2 are not working together, the trains are stopped.”

The researchers tested this idea by genetically modifying mice with SAVI, but without producing the ArfGAP2 protein. They found that the lung- and limb-destroying immune response typical of the disease did not occur, confirming that neutralizing this protein could turn off the overactive immune response.

This breakthrough has significant implications for treating other conditions that lead to excess immune proteins, such as cytokine storms in COVID-19 or brain inflammation linked to immune responses in Alzheimer’s disease. As Jonathan Miner, an associate professor at Penn’s Colter Center for Autoimmunity, said, “Diseases like SAVI that are super rare can provide valuable insights… Suddenly you’ve opened the doors to all these new avenues of potential therapies for many, many different classes of diseases.”