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Prepublished online as a Blood First Edition Paper on October 10, 2002; DOI 10.1182/blood-2002-05-1488.
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Blood, 1 March 2003, Vol. 101, No. 5, pp. 1898-1904
IMMUNOBIOLOGY
Non-IgE-dependent activation of human lung- and cord
blood-derived mast cells is induced by eosinophil major basic protein
and modulated by the membrane form of stem cell factor
Adrian M. Piliponsky,
Gerald J. Gleich,
Arnon Nagler,
Ilan Bar, and
Francesca Levi-Schaffer
From the Department of Pharmacology, School of
Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem,
Jerusalem, Israel; Departments of Immunology and Medicine,
Mayo Clinic and Foundation, Rochester, MN; Department of Bone Marrow
Transplantation, The Chaim Sheba Medical Center, Tel-Hashomer,
Israel and Department of Thoracic Surgery, Assaf Harofeh
Medical Center, Zerifin, Israel.
The allergic reaction begins with the antigen-induced aggregation
of occupied high-affinity IgE receptors expressed on mast cell surface,
their activation, and the release of proinflammatory mediators that
cause the "early phase" of this process. In addition, mast cell
activation induces the onset of a "late phase" reaction characterized by the tissue infiltration of inflammatory cells, mainly
eosinophils. We have hypothesized that during the late phase mast cells
interact with and are activated by eosinophils. Here we report that
highly purified human lung mast cells became responsive to eosinophil
major basic protein (MBP) when in coculture with human lung
fibroblasts. In addition, cord blood-derived mast cells maintained in
coculture with 3T3 fibroblasts released more histamine and
prostaglandin D2 (PGD2) compared with cells
maintained in suspension. The fibroblast-derived membrane form of stem
cell factor (SCF) was found to be involved in the mast cell increased responsiveness to MBP. In fact, cord blood-derived mast cells cocultured with 3T3 in the presence of antisense for SCF or cocultured with fibroblasts that do not express the membrane form of SCF were
inhibited in their histamine-releasing activity toward MBP. In
addition, this form of SCF induced the expression of a pertussis toxin-sensitive Gi protein, Gi3 that interacts
with MBP to trigger mast cell non-IgE-dependent activation in a manner
similar to other cationic compounds such as compound 48/80. Mast cell
responsiveness to eosinophil mediators is a potentially novel evidence
for an alternative pathway of allergen-independent activation able to contribute to the perpetuation of allergy.
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