DCs (blue) exposed to pollen lipids polarize T cells (yellow) toward a Th2 phenotype.

This group had discovered previously that pollen grains rapidly liberate eiconasoid-like substances, which are similar to prostaglandins and leukotrienes, when in an aqueous environment. These lipids bound to neutrophils and eosinophils (both involved in allergies and other immune reactions) and induced their activation, leading the group to propose that the release of these lipid mediators is an important event in allergic sensitization. What these data did not explain, however, was how the adaptive immune system becomes biased toward an allergy-inducing Th2 response.Traidl-Hoffmann et al. now show that soluble extracts from birch pollen and other common allergens inhibit the production of interleukin (IL)-12—the key cytokine involved in inhibiting Th2 responses—from activated DCs. These DCs could in turn bias naive T cells into becoming typical allergy-promoting Th2 cells.

Biochemical analysis of these extracts allowed the authors to identify the culprit of the IL-12 inhibitory activity: a group of prostaglandin-like compounds called E1 phytoprostanes (PPE1). These results fit nicely with the known Th2-polarizing effect of human prostaglandin E2 (PGE2) on DCs. The signaling pathways are not identical, however, as PGE2, but not PPE1, also inhibits tumor necrosis factor (TNF) and IL-10.

The function of these lipids in the plant is not completely clear, but they may be triggered in response to stress, as pollen exposed to air pollutants produce more of these compounds than do pollen from unpolluted areas. This may help explain why allergies are more prevalent in areas with high levels of car exhaust emissions. The authors are now looking for the receptor this compound uses to bind DCs. They also plan to assess whether DCs from allergy-prone individuals are more sensitive to the effects of PPE1 than those from nonallergic individuals.