In the next few slides, I just want to walk you through a very simplistic understanding of the type two inflammation in asthma. As you know, allergens, pollutants, and microbes, their exposure to the airway epithelium results in downstream inflammation. And there are three epithelial cytokines that have become recognized recently. These are also called alarmins, and these are interleukin 33, 25, and TSLP, or thymic stromal lymphopoietin. Now, dendritic cells are the antigen-presenting cells, and they then work on the naive T-helper cell and convert it to T-helper cell two that then mediates the allergic pathway or allergic inflammation that is also associated with eosinophilia. Through the interleukin 4 and 13, it causes activation of the B-cell class switching production of IgE. And as you know, IgE results in significant allergic inflammation by degranulation of mast cell and its effect on basophils. So this is a pathway for allergic asthma. The Th2 cell also secretes interleukin 5 that directly works on eosinophils. It participates in eosinophil maturation and survival and results in eosinophilic inflammation. And then interleukin 13 can cause mucus hypersecretion by its effects on goblet cells and also airway hyperresponsiveness by its effect on airway smooth muscles. Now, over the last decade, we've also become aware that there's innate immune cells that are participating in this type two inflammation. So Th2 is your adaptive pathway, and then the innate lymphoid cell type two, or Ilc2, is your adaptive, sorry, innate pathway. And that secretes interleukin 5 and 13 and resulting in the same end result of eosinophilic inflammation, airway hyperresponsiveness, and mucus hypersecretion that we discussed.

type 2 inflammation

asthma

interleukins

eosinophils

mucus hypersecretion