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-Inducible Protein of 10 kDa (CXC Chemokine Ligand (CXCL) 10) but Not Monokine Induced by IFN- (CXCL9) Imprints a Pattern for the Subsequent Development of Autoimmune Disease 1
* Department of Developmental Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121;
Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037; and
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129
Infection of the pancreas with lymphocytic choriomeningitis virus results in rapid and differential expression among CXCR3 chemokines. IFN-
-inducible protein of 10 kDa (IP-10), in contrast with monokine induced by IFN- and IFN-inducible T cell-
chemoattractant, is strongly expressed within 24 h postinfection. Blocking of IP-10, but not monokine induced by IFN-, aborts severity of Ag-specific injury of pancreatic 
cells and abrogates type 1 diabetes. Mechanistically, IP-10 blockade impedes the expansion of peripheral Ag-specific T cells and hinders their migration into the pancreas. IP-10 expression was restricted to viruses infecting the pancreas and that are capable of causing diabetes. Hence, virus-induced organ-specific autoimmune diseases may be dependent on virus tropism and its ability to alter the local milieu by selectively inducing chemokines that prepare the infected tissue for the subsequent destruction by the adaptive immune response.
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