Reversible immune abnormality and regulatory T cells in offspring of Der p 1-exposed female mice.

BACKGROUND Maternal allergic diseases have an important influence on the origin of allergic rhinitis (AR) in offspring, but the mechanism and the duration of the maternal effect are unknown. Previous researches prompted the important roles of Tregs and Foxp3 DNA methylation in the development of allergic diseases. OBJECTIVE To investigate the immune state and Tregs in the offspring of Der p 1-exposed female mice. METHOD BALB/c female mice were exposed to Der p1 to construct the mouse AR model, then mated with normal male mice. Offspring were kept in an allergen-free environment after birth. At postnatal weeks 3, 5 and 8, mice were culled for testing. RESULT Compared with the offspring of PBS-exposed female mice (N-N), the offspring of Der p 1-exposed female mice (A-N) showed increased IL-4 and decreased IL-10 levels in serum at postnatal weeks 3 and 5. Correspondingly, the percentage of Tregs in spleen CD4+ cells declined significantly at postnatal week 5 in A-N. Further analysis of the methylation status of spleen lymphocytes revealed hypermethylation of the Foxp3 promoter in A-N mice at postnatal weeks 3 and 5. However, by 8 weeks of age, all abnormalities in cytokines, Treg counts and Foxp3 DNA methylation in A-N mice had returned to normal levels. CONCLUSION Under the influence of maternal AR, offspring have an abnormal immune state at birth. However, without exposure to allergens, the immune state in AR offspring recovered by maturity. Changes in Tregs and Foxp3 DNA methylation may be the mechanism for this reversible immune abnormality in AR offspring.