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(CXC Chemokine Ligand 9) Is Made by APCs, Targets Lymphocytes Including Activated B Cells, and Supports Antibody Responses to a Bacterial Pathogen In Vivo
* Inflammation Biology Section and
Immune Cell Interaction Unit, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases,
Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, and
Division of Bacterial, Parasitic, and Allergenic Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892;
¶ Experimental Medicine and Inflammation Pharmacology, Pfizer Global R&D, Ann Arbor, MI 48105; and
|| Department of Immunology Research, Merck Research Laboratories, Rahway, NJ 07065
Monokine induced by IFN-
(Mig; CXC chemokine ligand 9) is an
IFN--inducible CXC chemokine that signals through the receptor CXCR3
and is known to function as a chemotactic factor for human T cells,
particularly following T cell activation. The mig gene
can be induced in multiple cell types and organs, and Mig has been
shown to contribute to T cell infiltration into immune/inflammatory
reactions in peripheral tissues in mice. We have investigated the
expression and activities of Mig and CXCR3 in mouse cells and the role
of Mig in models of host defense in mice. Murine (Mu)Mig functioned as
a chemotactic factor for resting memory and activated T cells, both
CD4+ and CD8+, and responsiveness to MuMig
correlated with surface expression of MuCXCR3. Using
mig-/- mice, we found that MuMig was not
necessary for survival after infections with a number of intracellular
pathogens. Surprisingly, however, we found that
mig-/- mice showed reductions of 50–75%
in Abs produced against the intracellular bacterium Francisella
tularensis live vaccine strain. Furthermore, we found that
MuMig induced both calcium signals and chemotaxis in activated B cells,
and that B cell activation induced expression of MuCXCR3. In addition,
IFN- induced the expression of mumig in APCs,
including CD8
+ and CD8- dendritic cells.
Together, our data suggest that Mig and CXCR3 may be important not only
to recruit T cells to peripheral inflammatory sites, but also in
some cases to maximize interactions among activated T cells, B cells,
and dendritic cells within lymphoid organs to provide optimal humoral
responses to pathogens.
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