Researchers at Trinity College in Dublin, Ireland have made a significant breakthrough in the treatment of allergic conditions, such as asthma and eczema. The team, led by Science Foundation Ireland Stokes Professor of Translational Immunology, Padraic Fallon, of the School of Medicine in the Trinity Biomedical Sciences Institute, demonstrated that a molecule, referred to as PD-L1, functions as a trigger to the inflammation characteristic of an allergic reaction in mice.

An allergic reaction occurs when the body’s immune system mistakes something (e.g., pollen and dust mites) for a pathogen and responds by taking measures to rid the body of that perceived threat. Treatment of allergies usually involves antihistamines, decongestants, and/or corticosteroids.

All of these medications operate by reducing allergic inflammation. Antihistamines, such as Benadryl or Claritin, block the action of the compound histamine. Histamine causes the inflammation symptoms characteristic of an allergic reaction, and is deployed by the immune system in an attempt to expel something from the body through the excess production of mucus. Decongestants, such as Sudafed and Afrin, and corticosteroids, such as Flonase and Nasacort, both function by reducing the inflammation that results from an allergic reaction.

While these three types of medication are effective at what they do, an allergic reaction is caused by a chain biochemical reaction within the body, and these drugs only stop said reaction at the end, or the symptomatic stage.

Fallon predicts that his team’s identification of the beginning of this chain reaction will be utilized by drug manufacturers to create medications that can halt allergic reactions at their origination, rather than at their conclusion. “This new discovery identifies a checkpoint that regulate the processes that start allergies at the early stages whereby cells talk to each other to instruct the immune system,” Fallon told The University Network (TUN).

Hence, blocking this checkpoint would stop the progression from the earliest cellular events that initiate allergies.

When asked what was next for this research, Fallon replied: “The next step is to address the clinical relevance of this discovery. Key questions to consider are, ‘is the same checkpoint happening in humans with allergies, can we block this response to prevent or delay the development of allergies in man?’”

If this biochemical checkpoint does in fact occur in humans as it does in mice, and a compound can be developed that blocks action at said checkpoint, then this research will revolutionize the way we think of allergies and how we treat them.

The full paper is published in The Journal of Experimental Medicine.

Dr. Christian Schwartz, Adnan R. Khan, Achilleas Floudas, Sean P. Saunders, Emily Hams, Hans-Reimer Rodewald, and Andrew N.J. McKenzie contributed to this research.