Blocking two immune molecules can prevent asthma attacks: a study

Blocking two immune molecules can prevent asthma attacks: a study

California: The La Jolla Institute for Immunology (LJI) has studied a new development, which has revealed the key to preventing asthma attacks by blocking two immune molecules at the same time, using a mouse model. It is important to avoid asthma attacks.
Asthma has become a major concern for Americans, as ten Americans die each day from the attack. Researchers have discovered a new way to relieve all asthma patients.
“We’ve found a way to stave off a severe inflammatory reaction to asthma,” said Michael Craft, a LJI professor and senior author of the new study, published November 5. There has been a permanent, lasting decline. ” 20 2020, in the Journal of Allergy and Clinical Immunology.
When an allergic person experiences an asthma stimulus, harmful T cells increase their numbers in the lungs and release the molecules that cause inflammation. New research shows how to throw the wrench in the process.
For the study, Croft Lab focused on blocking OX40L and CD30L, which indicate proteins similar to the tumor necrosis factor (TNF), a protein that is the target of several FDA-approved drugs. These molecules are aprogulated by allergens and can activate harmful T cells that trigger asthma inflammation.
In the new research, Kraft and his colleagues worked with a mouse model that is sensitive to household dust particles. It is a very common cause of allergies and asthma. Scientists have shown that inhibiting Aux 40L and CD30L at the same time can prevent the expansion and accumulation of harmful T cells in the lungs during an allergen attack, and subsequently reduce inflammation.
“Combining two sets of signals can drastically reduce the number of these pathogenic T cells, while neutralizing just one of the two has a relatively mild effect,” says Kraft. “It simply came to our notice then.
Importantly, blocking both OX40L and CD30L has also reduced the number of pathogenic T cells that travel to the lungs after an asthma attack. These “memory” T cells usually trigger inflammation when a person is exposed to allergens again. Without OX40L and CD30L at work, very few of these harmful T cells get trapped in the lungs, and mice had a weak response to household dust particles for weeks after initial treatment. “It simply came to our notice then that we were lowering the immune system of the allergen,” says Kraft.
The study comes years after an ineffective clinical trial targeting OX40L. Previous research by Craft Lab and other researchers suggested that blocking signaling with OX40L could reduce airway inflammation, yet neutral antibodies against OX40L could cause house dust mites or cat allergic asthma. May not have a beneficial effect in patients with “Why did it fail?” Kraft asks. “The new study supports the idea that simply blocking the OX40L was not enough.”
This study sheds light on the complexity of the immune system and suggests that long-term therapy in inflammatory and autoimmune diseases may require multidimensional approaches, especially when the number of pathogenic T cells Try to limit who is their main driver. Diseases
Testing a combination treatment to prevent both molecules would be complicated (researchers will need to prove the safety of blocking each one separately) but Kraft believes that either dual antibodies or “two specific” reagents OX40L and The CD30L can work simultaneously to prevent signaling. A cure
Craft is now thinking about the next steps in his lab. Blocking OX40L and CD30L reduced memory T cells but did not eliminate them all. Kraft believes that additional target molecules will be present. “We’re trying to figure out what that molecule could be,” Kraft said.

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