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CUTTING EDGE |
,§
,§,§,¶
Departments of
*
Medicine,
Pediatrics, and
Pathology, Harvard Medical School;
§
Division of Rheumatology, Immunology, and Allergy, Brigham and Women’s Hospital; and
¶
Partners Asthma Center, Boston, MA 02115
Tissue mast cell development requires stem cell factor (SCF),
whereas helminth-induced intestinal mucosal mast cell hyperplasia also
requires T cell-derived factors such as IL-3. We generated progenitor
mast cells (PrMC) from mouse bone marrow cells (BMC) in vitro with a
triad of SCF, IL-6, and IL-10 that exhibit IL-3-mediated mitogenic and
maturation responses. SCF/IL-6/IL-10 transiently elicited a cell
subpopulation with the phenotype
(c-kithighThy-1low) of fetal
blood promastocytes at 3 wk of culture that progressed within 1 wk to
Fc
RI-bearing PrMC, designated PrMCTriad.
PrMCTriad lacked mouse mast cell carboxypeptidase A
(mMC-CPA) protein, required SCF for IL-3-driven thymidine
incorporation, and responded to SCF plus IL-3 with strong mMc-CPA
immunoreactivity, clarifying distinct sequential roles for SCF and IL-3
in mast cell development. PrMCTriad, arising from BMC
through promastocytes, are metamastocytes that acquire
microenvironmentally determined phenotypic
features.
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