Taken together, our findings suggest that PAG suppressed Th2 immune responses through, at least partially, stimulating the secretion of IL-10 in food allergy mice.
On days 7-10, in EW-fed D10 and RD10 mice, splenic CD4+ T cells produced significantly more IL-4 than did those in the mesenteric lymph nodes (MLNs); this is in contrast to the excessive IL-4 response in the MLNs of EW-fed OVA23-3 and R23-3 mice.
The mRNA levels of the inflammatory cytokines interleukin-4 and tumor necrosis factor-α, and inflammatory cell infiltration in mouse colons were significantly decreased in hUC-MSCs-treated animals compared with mice with OVA-induced food allergy.
After being passively transferred with CAP-DCs or injection of scFv-IC, Ag-specific IL-17+ Foxp3+ iTregs were induced in the intestinal lamina propria of FA mice.
Mechanistic studies in mouse models of food allergy have confirmed that the composition of the intestinal microbiota can imprint susceptibility or resistance to food allergy on the host and have identified a unique population of microbially responsive RORγt-positive FOXp3-positive regulatory T cells as critical for the maintenance of tolerance to foods.
The ratio of Foxp3 mRNA to Foxp3 cells was decreased in patients with FA and in patients with celiac disease compared with controls (P = 0.036, P = 0.035).
On day 28, in EW-fed OVA23-3 and R23-3 mice, expression of Foxp3 on CD4+ T cells corresponded with recovery from inflammation, but recurrence of weight loss was observed on restarting the EW diet after receiving the control-diet for 1 month.No recurrence developed in D10 mice.
The lowest mean level of FOXP3 mRNA expression (1.9 ± 1.6) was recorded in children with asthma and FA, and the highest level (4.2 ± 4.2) was recorded in healthy children without atopy (P = .036).
To induce food allergy, wild-type (WT) and mice deficient for STAT-6 (Stat6<sup>-/-</sup>) were sensitized with peanut proteins and challenged with peanut seeds.
IgE-mediated FA was induced in BALB/c mice by oral gavage with medium-chain triglycerides (MCTs) plus egg white (EW) and was characterized by increased numbers of lamina propria T<sub>H</sub>2 cells, mast cells, and eosinophils, shock (hypothermia), mast cell degranulation (increased serum mouse mast cell protease 1), increased serum IgG<sub>1</sub> anti-EW and IgE levels, and increased IL-4 and IL-13 secretion after MCT/EW challenge.
To investigate a local production of IgE in intestine, we analysed the levels of transcripts for epsilon germ-line (epsilonGT), and potential regulators of IgE production, IL-4, IL-13, IFN-gamma, IL-4Ralpha, STAT6 and FcepsilonRIalpha in intestinal mucosa of adult patients with FA.
Here, we described the correlation between four genes [interleukin (IL)-4 (C-590T), IL-4 receptor (A1652G), FCER1B (G6842A) and STAT6 (G2964A)] in connection with IgE production; the role of IL-10 (C-627A) as a regulatory cytokine of allergy; and the severity of food allergy (FA) and atopic eczema (AE) in 220 Japanese allergic children.
Development of a BALB/c mouse model for food allergy: comparison of allergy-related responses to peanut agglutinin, β-lactoglobulin and potato acid phosphatase.
Taken together, our results demonstrated that BLG sensitization elicits inflammatory responses in the intestine and brain without overt anaphylactic signs of milk allergy, signifying food allergy as a potential pathogenic factor of neuropsychiatric disorders.
Here, we sought to investigate whether genetic polymorphisms at IL13 are associated with the development of challenge-proven IgE-mediated food allergy.
This study suggests that glycation of BLG by MR significantly alters its fate in processes involved in immunogenicity and allergenicity, pointing out the importance of food processing in food allergy.