Hippokratia 1997, 1(1):15-23
Several lines of evidence derived from animal and human models indicate that Th2-lymphocytes, mast cells, eosinophils, basophils and epithelial cells, importantly contribute to the pathogenesis of both acute and chronic components of allergic inflammation in asthma. Each of these cells represents a source of multiple cytokines and mediators that may have overlapping, synergistic, or even antagonistic effects. Some of the cells and mediators, that participate in the inflammatory process may help to down regulate the reaction, while cytokines that mediate certain proinflammatory effects may have other actions that are anti-inflammatory. Yet, despite these important changes in our thinking about the nature of allergic asthma, a complete understanding of the mechanisms that initiate and perpetuate the mucosal inflammation in this disease have proven to be quite elusive. The “riddle of the allergic reaction”, remains to be completely solved.