While inhalers are the go-to method for treatment during an asthma attack, a recent study has found a possible key to preventing other attacks from happening.

In a study of mice, researchers at La Jolla Institute for Immunology have found that blocking two immune molecules simultaneously is key to preventing asthma attacks.

“We have found a way to block the acute asthmatic inflammatory response — and we saw a strong, long-lasting reduction in asthma exacerbations,” Michael Croft, Ph.D., professor at LJI and senior author said in a press release from Science Daily.

The new study, which was published earlier this month in “The Journal of Allergy and Clinical Immunology,” saw researchers working with a mouse model sensitive to house dust mites, which is a very common trigger of asthma and allergies. Croft’s lab focused on blocking the signaling proteins OX40L and CD30L, which are similar to tumor necrosis factor (TNF). That protein is the target of several FDA-approved drugs.

The study showed blocking the two signaling proteins simultaneously could stop the expansion and accumulation of harmful T cells in the lungs during an allergen attack. As a result, inflammation was diminished.

“The combination of taking out the two sets of signals allowed for a strong reduction in the number of those pathogenic T cells, whereas only neutralizing either one had a relatively mild effect,” Croft said. “That was quite a significant finding.”

Additionally, blocking the signaling proteins decreased the number of pathogenic T cells that remained in the lungs once the asthma attack ceased. Normally, the “memory” T cells would induce inflammation the next time a person encounters an allergen. With OX40L and CD30L blocked, very few of the harmful T cells stayed in the lungs. Weeks after treatment, mice also had a weaker response to house dust mites.

Croft said the results suggest “we were diminishing the immune memory of the allergen.”

For more on the study, including what it shows about the immune system, read the press release here.

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