In addition to being a major effector cell in the elicitation of allergic i
nflammation, mast cells have been found to be activated in various T cell-m
ediated inflammatory processes and to reside in close physical proximity to
T cells, Such observations and the wide spectrum of mediators produced and
secreted by mast cells have led investigators to propose a functional rela
tionship between these 2 cell populations. Indeed, mast cell activation has
been reported to induce T-cell migration either directly by the release of
chemotactic factors, such as lymphotactin or IL-16, or indirectly by the i
nduction of adhesion molecule expression on endothelial cells, Mast cells a
re also able to present antigens to T cells, resulting in their activation
in either an MHC class I- or class II-restricted and costimulatory molecule
-dependent fashion. Adhesion molecule-dependent intercellular contact or MH
C class II cognate interactions between T cells and mast cells result in th
e release of both granule-associated mediators and cytokines from the latte
r, Also, T cell-derived mediators, such as beta-chemokines, directly induce
mast cell degranulation, On the other hand, mast cell-derived cytokines, s
uch as IL-4, have been found to polarize T cells to preferentially differen
tiate into the T-H2 subset. Thus T cell-mast fell interactions are bidirect
ional, fulfilling regulatory and/or modulatory roles affecting various aspe
cts of the immune response.