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1
*
Department of Medicine, Meir General Hospital, Kfar-Saba, Israel;
Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; and
Department of Immunology, Weizmann Institute of Science, Rehovot, Israel
Mast cells, essential effector cells in allergic inflammation, have
been found to be activated in T cell-mediated inflammatory processes in
accordance with their residence in close physical proximity to T cells.
We have recently reported that mast cells release granule-associated
mediators and TNF-
upon direct contact with activated T cells. This
data suggested an unrecognized activation pathway, where mast cells may
be activated during T cell-mediated inflammation. Herein, we show that
this cell-cell contact results in the release of matrix
metalloproteinase (MMP)-9 and the MMP inhibitor tissue inhibitor of
metalloproteinase 1 from HMC-1 human mast cells or from mature
peripheral blood-derived human mast cells. The expression and release
of these mediators, as well as of 
-hexosaminidase and several
cytokines, were also induced when mast cells were incubated with cell
membranes isolated from activated, but not resting, T cells.
Subcellular fractionation revealed that the mature form of MMP-9
cofractionated with histamine and tryptase, indicating its localization
within the secretory granules. MMP-9 release was first detected at
6 h and peaked at 22 h of incubation with activated T cell
membranes, while TNF- release peaked after only 6 h.
Anti-TNF- mAb inhibited the T cell membrane-induced MMP-9 release,
indicating a possible autocrine regulation of MMP release by mast cell
TNF-. This cascade of events, whereby mast cells are activated by T
cells to release cytokines and MMP-9, which are known to be essential
for leukocyte extravasation and recruitment to affected sites, points
to an important immunoregulatory function of mast cells within the
context of T cell-mediated inflammatory
processes.
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