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Receptors Induces the Expression of Macrophage-Inflammatory Protein (MIP)-1
, MIP-1
, and RANTES1
* Instituto de Biología y Genética Molecular, Consejo Superior de Investigaciones Científicas, and
Unidad de Investigación, Hospital Clínico Universitario, Valladolid, Spain
Monocytic cells were stimulated with IgG-OVA equivalence immune
complexes, mAb reacting with Fc
RI, FcRIIA, and FcRIII, LPS,
TNF-
, and the combination of ionomycin and phorbol ester, to address
their effects on the expression of the mRNAs encoding for chemokines.
Stimulation of monocytes with immune complexes induced a rapid
expression of macrophage-inflammatory protein (MIP)-1, MIP-1
, and
IL-8 mRNAs. In contrast, RANTES mRNA was already detectable in resting
cells and only increased after 16 h of stimulation. A similar
pattern was observed following homotypic stimulation of FcR with mAb
reacting with FcRI and FcRIIA, but not with a mAb reacting with
FcRIII, a subtype of receptor not expressed in THP-1 cells, thus
indicating that both FcRI and FcRIIA are involved in the
response. The pattern of chemokine induction elicited by LPS and the
combination of ionomycin and PMA showed some similarities to those
produced by FcR cross-linking, although expression of
IFN--inducible protein 10 mRNA was also observed in response to
those agonists. The production of MIP-1, MIP-1, and RANTES
proteins encompassing the induction of their mRNAs was confirmed by
specific ELISA. Experiments to address the transcription factors
involved in the regulation of MIP-1 using pharmacological agents and
EMSA showed the possible involvement of CCAAT/enhancer-binding protein
sites and ruled out the functional significance of both NF-AT and
AP-1 sites.
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