Asthma has long been a formidable foe for many people, causing symptoms that can range from mild discomfort to life-threatening attacks. While powerful biological drugs have significantly improved the lives of those with severe asthma, a recent study has shed light on why these symptoms often return despite treatment.

Biological drugs, or biologics, have become a crucial tool in managing severe asthma by helping patients keep their symptoms under control. However, researchers at Karolinska Institutet in Sweden discovered that certain immune cells, which play a significant role in asthma inflammation, do not disappear during treatment as previously thought. Instead, these inflammatory cells increase in number.

This finding suggests that biologics might not address the root cause of asthma, but rather manage its symptoms. As such, continued treatment may be necessary to keep the disease under control. This is particularly concerning considering that little is still known about the long-term effects of biologics like mepolizumab and dupilumab, which have been prescribed to asthmatics for less than ten years.

The study analyzed blood samples from 40 patients before and during treatment, using advanced methods such as flow cytometry and single-cell sequencing. Researchers were surprised to find that the levels of inflammatory cells in these patients increased rather than decreased. This could explain why inflammation of the airways often returns when the treatment is tapered or discontinued.

It is essential for researchers and medical professionals to understand the long-term immunological effects of biologics, as this knowledge can lead to more effective treatments and better outcomes for patients with severe asthma. The next stage of the study will involve analyzing samples from patients with a long treatment history and studying lung tissue to see how immune cells are affected in the airways.

The findings of this study have significant implications for the management and treatment of asthma, highlighting the need for continued research into the effects of biologics on the immune system.

The scientific community has long been aware that children growing up in urban areas are more prone to allergies than their rural counterparts. However, the exact reasons behind this disparity have remained unclear until recently. A groundbreaking study published in the journal Allergy sheds new light on how environmental factors shape the immune system and contribute to the increased risk of allergic diseases in urban children.

Researchers from the University of Rochester Medical Center (URMC) Department of Pediatrics discovered a previously uncharacterized subset of immune cells known as helper 2 (Th2) cells that play a critical role in the development of allergic diseases. These aggressive Th2 cells are more inflammatory than any other type of T-cell, and their presence is associated with an increased likelihood of developing allergies.

The study compared blood samples from urban infants with those from infants living in a farming community, known for its low rates of allergies. The findings revealed that while urban infants had higher levels of aggressive Th2 cells, the farming infants had more regulatory T-cells that help keep the immune system in balance and reduce the likelihood of allergic responses.

The lead researcher, Dr. Kirsi Järvinen-Seppo, speculates that differences in the development of the gut microbiome between the two populations may be a key factor contributing to this disparity. She suggests that exposure to “healthy” bacteria in rural environments may promote the development of a more tolerant immune system, while urban environments may prime immune cells for allergic inflammation.

This study is part of a broader investigation into how early-life exposures influence long-term immune outcomes. The researchers received a $7 million grant from the National Institute of Allergy and Infectious Diseases (NIAID) to continue their work in identifying protective factors that could be translated into preventive therapies, including probiotics or microbiome-supporting interventions.

The discovery of these aggressive Th2 cells and their association with urban allergies provides new insight into how environmental factors shape the immune system. As researchers continue to explore this area, they may uncover solutions to prevent allergic disease development in at-risk children.

Now, let’s dive into the rewritten article:

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.