Table 1.

Activated cell types and eosinophils that perpetuate airway inflammation

Cell type	Products produced	Biologic effect
Airway epithelium	TSLP, IL-33, IL-25	Respond to environmental insults through PRRs (see Box 2), activate dendritic cells
Dendritic cell	Processed antigen	Migrate to local lymph nodes and present antigen to expand TH2-type T cell population
TH2 lymphocyte	IL-4	Promotes B cell isotype switching, production of eotaxin, induces airway goblet cell metaplasia, amplifies airway epithelial response to environmental insults
	IL-13	Shares receptor with IL-4 and has similar biologic effects, may play a more important role in asthma compared to IL-4
	IL-5	Promotes eosinophil growth, maturation, and activation
B cell	Processed antigen, IgE	Activate T cells to reinforce IgE production, activate mast cells and eosinophils to release preformed products that characterize the early allergic response
Mast cell	Histamine, neutral proteases, lipid mediators	Increase vascular permeability and smooth muscle contraction resulting in airway hyperreactivity
	IL-4, IL-13, IL-5	Amplifies development and recruitment of mast cells to the lung
Eosinophil	Major basic protein	Toxic to bacteria and helminthes, but damage host cell membranes as well, may increase recruitment of other inflammatory cells
	IL-4, IL-13, IL-5	Amplifies development and recruitment of eosinophils to the lung
Airway smooth muscle	RANTES, eotaxin, IL-8, MCP, IL-5, ICAM/VCAM	Promotes activation and recruitment of inflammatory cells including mast cells and eosinophils, may promote matrix deposition and hypertrophy