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Receptor-Deficient Mice1
Laboratories of
*
Immunobiology,
Experimental Chemotherapy, and
Molecular Immunology, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium; and
AnorMed, Langley, British Columbia, Canada
Autoimmune collagen-induced arthritis (CIA) in IFN-
R-deficient
DBA/1 mice was shown to be reduced in severity by treatment with the
bicyclam derivative AMD3100, a specific antagonist of the interaction
between the chemokine stromal cell-derived factor-1 (SDF-1) and its
receptor CXCR4. The beneficial effect of the CXCR4 antagonist was
demonstrable when treatment was initiated between the time of
immunization and appearance of the first symptoms. Treatment also
reduced the delayed-type hypersensitivity response to the autoantigen,
collagen type II. These observations are indicative of an action on a
late event in the pathogenesis, such as chemokine-mediated attraction
of leukocytes toward joint tissues. The notion of SDF-1 involvement was
further supported by the observation that exogenous SDF-1 injected in
periarthritic tissue elicited an inflammatory response that could be
inhibited by AMD3100. The majority of leukocytes harvested from
inflamed joints of mice with CIA were found to be Mac-1+
and CXCR4+, and AMD3100 was demonstrated to interfere
specifically with chemotaxis and Ca2+ mobilization induced
in vitro by SDF-1 on Mac-1+/CXCR4+ splenocytes.
We conclude that SDF-1 plays a central role in the pathogenesis of
murine CIA, by attracting Mac-1+/CXCR4+ cells
to the inflamed joints.
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