PMID- 9274861
OWN - NLM
STAT- MEDLINE
DCOM- 19970911
LR  - 20130118
IS  - 0023-6837 (Print)
IS  - 0023-6837 (Linking)
VI  - 77
IP  - 2
DP  - 1997 Aug
TI  - Production of macrophage inflammatory protein-1alpha by human mast cells: 
      increased anti-IgE-dependent secretion after IgE-dependent enhancement of mast 
      cell IgE-binding ability.
PG  - 185-93
AB  - 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 epsilonRI) 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-1alpha 
      (MIP-1alpha). 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-1alpha 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 epsilonRI-dependent challenge with significantly increased 
      secretion of MIP-1alpha, a chemokine that can have diverse functions in 
      inflammation, allergic reactions, and host responses to infection.
FAU - Yano, K
AU  - Yano K
AD  - Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical 
      School, Boston, Massachusetts 02215, USA.
FAU - Yamaguchi, M
AU  - Yamaguchi M
FAU - de Mora, F
AU  - de Mora F
FAU - Lantz, C S
AU  - Lantz CS
FAU - Butterfield, J H
AU  - Butterfield JH
FAU - Costa, J J
AU  - Costa JJ
FAU - Galli, S J
AU  - Galli SJ
LA  - eng
GR  - AI/CA-23990/AI/NIAID NIH HHS/United States
GR  - CA/AI-72074/CA/NCI NIH HHS/United States
GR  - HL-56383/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Lab Invest
JT  - Laboratory investigation; a journal of technical methods and pathology
JID - 0376617
RN  - 0 (Antibodies, Anti-Idiotypic)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (anti-IgE antibodies)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Antibodies, Anti-Idiotypic/*physiology
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Histamine Release
MH  - Humans
MH  - Immunoglobulin E/*physiology
MH  - Macrophage Inflammatory Proteins/*biosynthesis
MH  - Mast Cells/*metabolism
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
PST - ppublish
SO  - Lab Invest. 1997 Aug;77(2):185-93.