In anti-CD3 stimulated cells, Se supplementation did not affect IL-4 and IL-10 production when compared to the positive control group (Determine S5). cell degranulation were decided upon whey challenge. Body temperature was significantly higher in mice that received the Eledoisin Acetate medium Se diet 60 min after the oral challenge with whey compared to the positive control group, which is usually indicative of impaired anaphylaxis. This was accompanied by reductions in antigen-specific immunoglobulins and reduced levels of mouse mast cell protease-1 (mMCP-1). This study demonstrates that oral Se supplementation may modulate allergic responses to whey by decreasing specific antibody responses and mMCP-1 release. Keywords:seleno-l-methionine, selenium, cows milk allergy, mouse model, dendritic cells, T cells, mMCP-1 == 1. Introduction == Cows milk allergy (CMA) is one of the most common food allergies, affecting 23% of all infants [1]. In IgE-mediated CMA, about 85% of patients mostly experience moderate symptoms, while 15% can develop severe allergic responses and about 9% develop anaphylaxis within minutes to hours after ingestion of cows milk [2,3]. Although 6075% of children with IgE-mediated CMA spontaneously develop tolerance to cows milk before their fifth year of life, the risk of developing other atopic disorders later in life, such as asthma, is usually increased [4]. At the moment, no curative treatment is usually available for CMA and the only way to prevent allergic reactions is usually to avoid the intake of cows milk proteins. Therefore, novel approaches to prevent or treat CMA are urgently needed. CMA is usually defined as an immunologically mediated adverse reaction to cows milk protein [5,6], which can result from a breakdown or a delay in the development of oral tolerance [7]. The major allergens in cows milk are S1-casein from casein, and -lactalbumin and -lactoglobulin from whey. These proteins can be degraded in the intestines and pass through the epithelial barrier, after which they are offered to nave T-cells by antigen-presenting cells such as dendritic cells (DC). In CMA, these T-cells differentiate into T helper 2 cells (Th2) which can drive allergic immune responses, including the growth of eosinophils and mast cells, as well as isotype switch in B cells towards IgE production [8]. A number of food allergen immunotherapies are under investigation; however, these are limited in their ability to restore immune tolerance to food allergens, and often result in high rates of allergic side effects [9]. dmDNA31 Nutritional interventions including omega-3 polyunsaturated fatty acids, prebiotics, probiotics, and symbiotic supplementation as well as Vitamin D have gathered more desire for the prevention, secondary prevention and treatment of food allergies [10,11]. With the accumulating knowledge of the involvement of micronutrients in immunological processes, there is increasing desire for the relationship between minerals and the development of immune responses. It is known that deficiencies in several minerals such as iron, zinc, copper and selenium (Se) may result in impaired and/or less efficient immune function but little is known about their specific role in food allergy development [6,12,13]. Se is usually a metalloid mineral which is considered to have significant potential to influence the immune system. For example, Se supplementation reduced inflammation in a Staphylococcus aureus-infected mouse mastitis model [14,15], and an increase in Se intake improved antigen-responsiveness in immune cells from adults [16]. Se has been demonstrated to improve the activation of chicken DCs in vitro [17], and dietary Se supplementation has been shown to favor differentiation of naive cluster of differentiation (CD)4+ T lymphocytes dmDNA31 towards T helper 1 cells (Th1) [18,19], supporting the acute cellular immune response. In addition, dietary Se increased the percentage of splenic regulatory T cells (Treg) [20]. Furthermore, in a mouse model for systemic lupus erythematosus, Se supplementation inhibited activation, differentiation and maturation of B cells and macrophages [21]. Lower serum levels of selenium have also been associated with several skin diseases including atopic dermatitis [22]. People suffering from allergic asthma have significantly lower Se concentrations in their blood than healthy individuals [23]. Se status is known to impact the function of the immune cells and their ability dmDNA31 to respond to antigens [24], which suggests that Se may influence allergic disease. Selenomethionine (SeMet) can be an organic type of Se, an important trace component that features in the rules of dmDNA31 the immune system response [25,26]. Dental SeMet administration suppressed ovalbumin-induced allergic sensitization inside a mouse model for energetic cutaneous anaphylaxis by decreasing Th2 cytokine creation and augmenting Th1 cytokine creation [27]. However, it isn’t known how SeMet impacts CMA. Since proof shows that organic Se, SeMet, is way better consumed by pets and human beings and includes a larger bioavailability than inorganic types of Se [28], it was looked into how CMA can be modulated by SeMet-enriched diet programs. == 2. Components and Strategies == == 2.1. Mice == Four-week-old, specific-pathogen-free feminine C3H/HeOuJ.