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*
Istituto Ricerche Farmacologiche Mario Negri, Milan, Italy;
Hôpital Cochin, Institut National de la Santé et de la Recherche Médicale (INSERM) U283, Paris, France;
Dipartimento Medicina Sperimentale e Patologia, Università La Sapienza, Rome, Italy;
§
Sanofi Recherches, Labège, France; and
¶
Dipartimento Biotecnologie, Univ. Brescia, Brescia, Italy
Monocyte chemotactic protein-3 (MCP-3) is a C-C chemokine that
interacts with the CCR1, CCR2, and CCR3 receptors and has a spectrum of
action encompassing T cells, NK cells, eosinophils, and dendritic cells
(DC), in addition to mononuclear phagocytes. This broad spectrum of
action prompted the present study aimed at assessing the antitumor
activity of MCP-3 in a gene transfer approach and at providing
information as to the actual in vivo leukocyte recruiting capacity of
MCP-3. P815 mastocytoma cells transfected with the gene coding MCP-3
(P815/MCP-3) grew in syngeneic hosts and underwent
rejection. Rejection was associated with profound alterations of
leukocyte infiltration and resistance to subsequent challenge with P815
cells. Tumor-associated macrophages, already present in copious
numbers, T cells, eosinophils, and neutrophils, increased in tumor
tissues after gene transfer. DC, identified as
DEC205+, high MHC class II+,
CD11c+ cells, did not increase substantially in the tumor
mass. However, in peritumoral tissues, DC accumulated in perivascular
areas. P815/MCP-3-transfected tumor cells grew normally in
nude mice. Increased accumulation of macrophages and polymorphonuclear
neutrophils was evident also in nude mice. mAb against CD4, CD8, and
IFN-
, but not against IL-4, inhibited rejection of
MCP-3-producing cells. An anti-polymorphonuclear mAb
caused only a retardation of MCP-3-elicited tumor rejection. Thus,
MCP-3 gene transfer elicits tumor rejection by activating
type I T cell-dependent immunity. It is tempting to speculate that
altered trafficking of APCs, which express receptors and respond to
MCP-3, together with recruitment of activated T cells, underlies
activation of specific immunity by MCP-3-transfected cells.
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