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(MIG), IFN-Inducible T Cell 
Chemoattractant (I-TAC), and IFN--Inducible Protein-10 (IP-10) Chemokines by Human Neutrophils1
Departments of
*
General Pathology and
Pediatric Clinic, University of Verona, Verona, Italy;
Molecular Biology and Cell Biology Department, Human Genome Sciences, Inc., Rockville, MD 20850; and
§
Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
Monokine induced by IFN-
(MIG), IFN-inducible T cell 
chemoattractant (I-TAC), and IFN--inducible protein of 10 kDa
(IP-10) are related members of the CXC chemokine subfamily that bind to
a common receptor, CXCR3, and that are produced by different cell types
in response to IFN-. We have recently reported that human
polymorphonuclear neutrophils (PMN) have the capacity to release IP-10.
Herein, we show that PMN also have the ability to produce MIG and to
express I-TAC mRNA in response to IFN- in combination with either
TNF- or LPS. While IFN-, alone or in association with agonists
such as fMLP, IL-8, granulocyte (G)-CSF and granulocyte-macrophage
(GM)-CSF, failed to influence MIG, IP-10, and I-TAC gene expression,
IFN-, in combination with TNF-, LPS, or IL-1ß, resulted in a
considerable induction of IP-10 release by neutrophils. Furthermore,
IL-10 and IL-4 significantly suppressed the expression of MIG, IP-10,
and I-TAC mRNA and the extracellular production of MIG and IP-10 in
neutrophils stimulated with IFN- plus either LPS or TNF-.
Finally, supernatants harvested from stimulated PMN induced migration
and rapid integrin-dependent adhesion of CXCR3-expressing lymphocytes;
these activities were significantly reduced by neutralizing
anti-MIG and anti-IP-10 Abs, suggesting that they were mediated
by MIG and IP-10 present in the supernatants. Since MIG, IP-10, and
I-TAC are potent chemoattractants for NK cells and Th1 lymphocytes, the
ability of neutrophils to produce these chemokines might contribute not
only to the progression and evolution of the inflammatory response, but
also to the regulation of the immune response.
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