In recent years, the emerging concept of bronchial inflammation as a p
rominent histopathologic characteristic of asthma has profoundly modif
ied the view of the role of the mast cell, which was traditionally tho
ught to be linked to the release of soluble chemical mediators substan
tially involved in the genesis of acute, immediate bronchospasm. The f
inding that the production of proinflammatory cytokines by mast cells
in asthmatic airways is comparable, in some circumstances, to that of
T-cell origin, has led to the hypothesis that mast cells, along with T
lymphocytes and eosinophils, may also contribute to the genesis of ch
ronic, persistent asthma. This hypothesis is further supported by the
finding that mast cells are able to functionally interact with B cells
(promoting IgE synthesis) and T lymphocytes (acting as antigen presen
ting cells), thus taking part in the immune network. Moreover, mast ce
lls produce an exclusive family of proteases (tryptases and chymases)
that exert many biological actions relevant to airways inflammation an
d remodeling. Future studies will better explain the role of mast cell
s in asthma and, more specifically, the links with bone marrow-where m
ast cell progenitors originate-and the airways, where mast cells devel
op, differentiate, and assume the functions of mature cells. This arti
cle reviews recent data available on these topics.