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Researchers have identified a possible mechanism by which house dust mites could trigger the development of atopic dermatitis in individuals with a genetic predisposition.
The study, published online Feb. 10 in Science Translational Medicine, took skin and blood samples from individuals with atopic dermatitis and healthy controls, then exposed the samples to house dust mite allergen.
They found that in individuals with atopic dermatitis, this exposure modified phospholipids in the skin to release lipid antigens that then drove T-cell reactivity and inflammation (Sci Transl Med. 2016 Feb 10. doi: 10.1126/scitranslmed.aad6833).
Furthermore, the study suggested that the skin barrier protein filaggrin can inhibit the modified phospholipid activity and decrease the skin inflammation caused by allergen exposure in atopic dermatitis; however, individuals with atopic dermatitis are more likely to have defective filaggrin.
“The data would support therapeutic approaches to inhibit allergen-derived PLA2 [phospholipase A2] activity, together with treatments that target the downstream immunological effector pathways,” wrote Dr. Rachael Jarrett of the University of Oxford (England) and coauthors.
The study was funded by the U.K. Medical Research Council and National Institute for Health Research Biomedical Research Centre, the National Institutes of Health, and the Burroughs Wellcome Fund in Translational Medicine. Several of the researchers acknowledged grants and pharmaceutical company support. No conflicts of interest were declared.
Researchers have identified a possible mechanism by which house dust mites could trigger the development of atopic dermatitis in individuals with a genetic predisposition.
The study, published online Feb. 10 in Science Translational Medicine, took skin and blood samples from individuals with atopic dermatitis and healthy controls, then exposed the samples to house dust mite allergen.
They found that in individuals with atopic dermatitis, this exposure modified phospholipids in the skin to release lipid antigens that then drove T-cell reactivity and inflammation (Sci Transl Med. 2016 Feb 10. doi: 10.1126/scitranslmed.aad6833).
Furthermore, the study suggested that the skin barrier protein filaggrin can inhibit the modified phospholipid activity and decrease the skin inflammation caused by allergen exposure in atopic dermatitis; however, individuals with atopic dermatitis are more likely to have defective filaggrin.
“The data would support therapeutic approaches to inhibit allergen-derived PLA2 [phospholipase A2] activity, together with treatments that target the downstream immunological effector pathways,” wrote Dr. Rachael Jarrett of the University of Oxford (England) and coauthors.
The study was funded by the U.K. Medical Research Council and National Institute for Health Research Biomedical Research Centre, the National Institutes of Health, and the Burroughs Wellcome Fund in Translational Medicine. Several of the researchers acknowledged grants and pharmaceutical company support. No conflicts of interest were declared.
Researchers have identified a possible mechanism by which house dust mites could trigger the development of atopic dermatitis in individuals with a genetic predisposition.
The study, published online Feb. 10 in Science Translational Medicine, took skin and blood samples from individuals with atopic dermatitis and healthy controls, then exposed the samples to house dust mite allergen.
They found that in individuals with atopic dermatitis, this exposure modified phospholipids in the skin to release lipid antigens that then drove T-cell reactivity and inflammation (Sci Transl Med. 2016 Feb 10. doi: 10.1126/scitranslmed.aad6833).
Furthermore, the study suggested that the skin barrier protein filaggrin can inhibit the modified phospholipid activity and decrease the skin inflammation caused by allergen exposure in atopic dermatitis; however, individuals with atopic dermatitis are more likely to have defective filaggrin.
“The data would support therapeutic approaches to inhibit allergen-derived PLA2 [phospholipase A2] activity, together with treatments that target the downstream immunological effector pathways,” wrote Dr. Rachael Jarrett of the University of Oxford (England) and coauthors.
The study was funded by the U.K. Medical Research Council and National Institute for Health Research Biomedical Research Centre, the National Institutes of Health, and the Burroughs Wellcome Fund in Translational Medicine. Several of the researchers acknowledged grants and pharmaceutical company support. No conflicts of interest were declared.
FROM SCIENCE TRANSLATIONAL MEDICINE
