Adoptively transferred allergen-specific T cells cause maternal transmission of asthma risk.

In addition to genetics and environment, maternal asthma is an identified risk factor for developing the disease during childhood. The mechanisms of this maternal effect remain poorly understood. We tested the role of allergen-specific T cells in the maternal transmission of asthma risk by modifying a model where offspring of asthmatic mothers are more prone to develop asthma after an intentionally suboptimal asthma induction. Normal BALB/c females were injected with allergen-specific T cells from ovalbumin-specific T cell receptor (TCR) transgenic DO11.10 donors before mating. Using the protocol of suboptimal asthma induction, offspring of normal and recipient mothers were tested for their susceptibility to develop asthma. Only pups of recipient mothers showed increased airway responsiveness (Penh), allergic airway inflammation with eosinophilia, and local Th2-skewed cytokine production. Although recipient mothers did not develop asthma, serum levels of interferon-gamma, interleukin (IL)-4, IL-10, and IL-13 were significantly increased during pregnancy. Consistent with this finding, a subset of DO11.10 T cells persisted in the spleen and placenta of expectant recipient mothers. We conclude that allergen-specific T cells are sufficient to orchestrate the maternal transmission of asthma risk. Because overt maternal asthma was not required, our results suggest that similar maternal-fetal interactions may occur in other allergic disorders.