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The innate immune system includes cells well known to be involved in food allergy such as mast cells, basophils, group 2 innate lymphoid cells (ILC2s) and dendritic cells (DCs Minnicozzi et al., 2011 Tordesillas et al., 2017). More recently, our understanding of the factors contributing to food allergy pathogenesis has grown to include epithelial barrier function and signaling ( Groschwitz and Hogan, 2009 Wesemann and Nagler, 2016), the host microbiota ( Feehley et al., 2019 Wesemann and Nagler, 2016), and the innate immune system ( Minnicozzi et al., 2011 Tordesillas et al., 2017). It has long been understood that IgE-mediated food allergies result from a type 2 helper T cell (Th2) immune response of the adaptive immune system to protein antigens associated with specific foods ( Akdis, 2006 Chiang et al., 2018 Sampson et al., 2018 Turcanu et al., 2003 Wambre et al., 2017 Wisniewski et al., 2015 Yu et al., 2016). Because of the life-threatening potential of anaphylaxis associated with IgE-mediated food allergies, this disease has become a significant public health problem and health cost burden ( Gupta et al., 2019). In support of this novel model, we show clinically that the initiation of oral immunotherapy (OIT) in peanut-allergic patients is associated with a decrease in CD209 + DCs, suggesting that breaking the cycle of positive feedback is associated with therapeutic effect.įood allergies affect ≤10% of children and adults in different countries around the globe, including the United States ( Gupta et al., 2018 Gupta et al., 2019), China ( Hu et al., 2010), Australia ( Osborne et al., 2011 Tang and Mullins, 2017), Honduras ( Gonzales-González et al., 2018), United Arab Emirates ( Al-Hammadi et al., 2010), Italy ( Asero et al., 2009 Caffarelli et al., 2011), and Poland ( Bartuzi et al., 2017 Steinke et al., 2007). CD209 + DCs act reciprocally on the same peanut-specific CD4 + T cell population to reinforce Th2 cytokine expression in a positive feedback loop, which may explain the persistence of established food allergy. Here, we show that in peanut-allergic humans, peanut allergen drives the differentiation of CD209 + monocyte-derived dendritic cells (DCs) and CD23 + (FcєRII) myeloid dendritic cells through the action of allergen-specific CD4 + T cells. However, little is known about the response of specific antigen-presenting cell (APC) subsets to food allergens in the setting of food allergies. No other disclosures were reported.įood allergies are a leading cause of anaphylaxis, and cellular mechanisms involving antigen presentation likely play key roles in their pathogenesis.
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10/064,936, issued ), and a patent to "microfluidic device and diagnostic methods for allergy testing based on detection of basophil activation" (US patent no.
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12/610,940, filed, issued ), a patent to "mixed allergen compositions and methods for using the same" (US patent no. 12/686,121, filed ), a patent to "methods and assays for detecting and quantifying pure subpopulations of white blood cells in immune system disorders" (US patent no. S10-392, filed ), a patent to "granulocyte-based methods for detecting and monitoring immune system disorders" (US application no. 62/119,014, filed 2/20/15, issued 8/15/17) issued, a patent to "basophil activation-based diagnostic allergy test" (US application no. 62/647,389, filed ), a patent to "special oral formula for decreasing food allergy risk and treatment for food allergy (US patent no. Nadeau had a patent to "inhibition of allergic reaction to peanut allergen using an IL-33 inhibitor" (US patent no. Nadeau reported grants from the National Institute of Allergy and Infectious Diseases, the National Heart, Lung, and Blood Institute, the National Institute of Environmental Health Sciences, and Food Allergy Research and Education "other" from World Allergy Organization, Cour Pharma, Before Brands, Alladapt, Latitude, IgGenix, Immune Tolerance Network, and the National Institutes of Health clinical research centers outside the submitted work. Mellins reported grants from Glaxo-Smith-Kline and Novartis outside the submitted work.