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Production
of Macrophage Inflammatory Protein-1 alpha by Human Mast Cells: Increased
Anti-IgE-Dependent Secretion after IgE-Dependent Enhancement of Mast Cell
IgE-Binding Ability |
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Tetsuya Matsumoto,
Kiyonobu Ikeda, Naofumi Mukaida, Akihisa Harada, Yoshihiro Matsumoto, Junkoh
Yamashita, and Kouji Matsushima |
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Departments
of Pathology (KY, MY, FM, CSL, JJC, SJG) and Medicine (JJC), Beth Israel
Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts;
and Division of Allergic Diseases (JHB), Department of Medicine, Mayo Clinic
and Mayo Foundation, Rochester, Minnesota |
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The contributions of mast
cells to the pathology of allergic diseases, as well as to the expression
of immunoglobulin E (IgE)-dependent host responses to parasites, reflect
both the amounts and types of cytokines and other mediators that are released
by these cells in such settings. Whereas mast cells cannot intrinsically
express immunologically specific functions, the binding of IgE to high-affinity
IgE receptors (Fc epsilon RI) on the surface of mast cells primes these
cells to secrete cytokines and other biologically active products upon subsequent
exposure to specific antigens. We now report that both HMC-1, a growth factor-independent
human mast cell leukemia cell line, and growth factor-dependent human umbilical
cord blood-derived mast cells can secrete the multifunctional C-C chemokine,
macrophage inflammatory protein-1 alpha (MIP-1 alpha). In addition, we found
that in vitro exposure of human umbilical cord blood-derived mast cells
to concentrations of IgE within the range observed in the serum of subjects
with allergic diseases or parasite infections, which markedly up-regulates
the ability of these cells to bind IgE to their surface, also significantly
enhances the ability of the cells to secrete MIP-1 alpha upon subsequent
passive sensitization with IgE and challenge with anti-IgE. Thus, IgE-dependent
enhancement of human mast cell IgE-binding ability permits these cells to
respond to Fc epsilon RI-dependent challenge with significantly increased
secretion of MIP-1 alpha, a chemokine that can have diverse functions in
inflammation, allergic reactions, and host responses to infection. |
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