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Why some people have allergies from dust mites and others don’t

Household allergens are common, but the way they affect people differs.

For some, encountering dust mites leads to itchiness, a runny nose and sneezing, while others remain unaffected. New research examines why this is the case to treat causes of allergies and asthma, which can be aggravated by allergic reactions.

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In a study recently published in the journal Science Immunology, La Jolla Institute for Immunology scientists have found part of the answer for why nonallergic people don’t have a severe reaction to house dust mites. A previously unknown subset of T cells has been uncovered. Those T cells may restrict allergic immune reactions and asthma from ever developing in response to  possible allergens, including house dust mites.

“We discovered new immune cell subsets and new therapeutic opportunities,” Grégory Seumois, instructor and director of LJI’s Sequencing Core and co-leader of the new study, said in a press release. “This new population of cells could be one, out of many unknown mechanisms, that explains why healthy people don’t develop inflammation when they breathe in allergens.”

LJI professor Pandurangan Vijayanand, senior author of the new study, added: “The study highlights the power of unbiased single-cell genomics approaches to uncover novel biology.”

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Using a method that’s part of the “genomic revolution” arsenal of tools, called single-cell RNA-seq (or single-cell transcriptomics), researchers saw precisely which genes and molecules specific T cells produce in response to house dust mite allergens. Cells from four groups of people were tested: healthy participants, participants who suffer from asthma and HDM allergy, people who suffer only from asthma and no HDM allergy, and people who only have an HDM allergy.

The examination indicated a subset of helper T cells, called interleukin-9 Th2 expressing HDM-reactive cells, is more widespread in the blood of people with HDM-allergic asthma compared with people who only have HDM allergies. More examinations showed IL9-TH2 cells could kill other cells and promote inflammation.

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On the other hand, another subset of T cells was prominent in nonallergic participants. The subset showed an “interferon response signature” and was enriched for a gene that encodes a protein called TRAIL. 

Researchers’ work indicates TRAIL could be important since it could lessen the triggering of helper T cells.

The findings could provide some insight as to why some people develop asthma and allergies and others don’t.

“Now if functional studies confirm this dampening effect, we’re curious if there is a way to boost the activation of these T cells or induce their proliferation in asthmatic or allergic populations,” Seumois said. “Can we act on those cells very early on, before asthma has developed?”

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