For a study, researchers wanted to investigate the most recent, most significant genetic and epigenetic alterations of the epithelial barrier in response to environmental variables that might cause asthma, such as allergens, viruses, and pollution. In practically all asthma research, polymorphisms in the IL-33 and TSLP genes are discovered. Recent research showed a novel subset of innate lymphoid cells that were activated by the two cytokines and mediate type 2 innate immunity-dependent asthma. Early virally infected high-risk birth cohorts were found to have gene variants of innate pattern recognition receptors associated with asthma, as well as polymorphisms in pathways involved in type I interferon (IFN) production, providing more insight into the role of viruses in asthma development. Novel epigenetic pathways in asthma and in response to environmental pollutants were discovered, pointing to genes like TSLP as possible links between environmental pollution and asthma.

The importance of a specific group of epithelium-derived proTh2 cytokines, including IL-33 and TSLP, as well as reduced type I IFN, in the virus-induced compromised epithelial barrier, is supported by genetic evidence. Epigenetic changes of epithelial genes are intriguing processes worth investigating further.