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-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis1
Departments of
* Immunology and
Morphological Sciences, and
Rappaport Family Institute for Research in the Medical Sciences, Bruce Rappaport Faculty of Medicine, Haifa, Israel
IFN-
-inducible protein 10 (IP-10) is a CXC chemokine that is
thought to manifest a proinflammatory role because it stimulates the
directional migration of activated T cells, particularly Th1 cells. It
is an open question whether this chemokine is also directly involved in
T cell polarization. We show here that during the course of
adjuvant-induced arthritis the immune system mounts a notable Ab titer
against self-IP-10. Upon the administration of naked DNA encoding
IP-10, this titer rapidly accelerates to provide protective immunity.
Self-specific Ab to IP-10 developed in protected animals, as well as
neutralizing Ab to IP-10 that we have generated in rabbits, could
inhibit leukocyte migration, alter the in vivo and in vitro Th1/Th2
balance toward low IFN-, low TNF-
, high IL-4-producing T cells,
and adoptively transfer disease suppression. This not only demonstrates
the pivotal role of this chemokine in T cell polarization during
experimentally induced arthritis but also suggests a practical way to
interfere in the regulation of disease to provide protective immunity.
From the basic science perspective, this study challenges the paradigm
of in vivo redundancy. After all, we did not neutralize the activity of
other chemokines that bind CXCR3 (i.e., macrophage-induced gene
and IFN-inducible T cell chemoattractant) and yet significantly
blocked not only adjuvant-induced arthritis but also the in vivo
competence to mount delayed-type
hypersensitivity.
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