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-Inducible Protein 10 (IP-10; CXCL10)-Deficient Mice Reveal a Role for IP-10 in Effector T Cell Generation and Trafficking1
*
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; and
Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697
IFN-
-inducible protein 10 (IP-10, CXCL10), a chemokine secreted
from cells stimulated with type I and II IFNs and LPS, is a
chemoattractant for activated T cells. Expression of IP-10 is seen in
many Th1-type inflammatory diseases, where it is thought to play an
important role in recruiting activated T cells into sites of tissue
inflammation. To determine the in vivo function of IP-10, we
constructed an IP-10-deficient mouse (IP-10-/-) by
targeted gene disruption. Immunological analysis revealed that
IP-10-/- mice had impaired T cell responses. T cell
proliferation to allogeneic and antigenic stimulation and IFN-
secretion in response to antigenic challenge were impaired in
IP-10-/- mice. In addition, IP-10-/- mice
exhibited an impaired contact hypersensitivity response, characterized
by decreased ear swelling and reduced inflammatory cell infiltrates. T
cells recovered from draining lymph nodes also had a decreased
proliferative response to Ag restimulation. Furthermore,
IP-10-/- mice infected with a neurotropic mouse hepatitis
virus had an impaired ability to control viral replication in the
brain. This was associated with decreased recruitment of
CD4+ and CD8+ lymphocytes into the brain,
reduced levels of IFN- and the IFN--induced chemokines monokine
induced by IFN- (Mig, CXCL9) and IFN-inducible T cell 
chemoattractant (I-TAC, CXCL11) in the brain, decreased numbers of
virus-specific IFN--secreting CD8+ cells in the spleen,
and reduced levels of demyelination in the CNS. Taken together, our
data suggest a role for IP-10 in both effector T cell generation and
trafficking in vivo.
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