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INFLAMMATION/IMMUNITY/MEDIATORS

Role of IP-10/CXCL10 in the progression of pancreatitis-like injury in mice after murine retroviral infection

Departments of ¹Gastroenterology and Hepatology and ³Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata; ⁵Department of Bacterial and Blood Products, National Institute of Infectious Diseases, Tokyo; ²Department of Molecular Preventive Medicine, University of Tokyo Graduate School of Medicine, Tokyo; ⁴Department of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, Niigata, Japan; and ⁶Department of Food Science and Technology, Yeungnam University, Gyeongsan, Republic of Korea

Submitted 4 January 2006 ; accepted in final form 1 April 2006

Exocrinopathy and pancreatitis-like injury were developed in C57BL/6 (B6) mice infected with LP-BM5 murine leukemia virus, which is known to induce murine acquired immunodeficiency syndrome (MAIDS). The role of chemokines, especially CXCL10/interferon (IFN)--inducible protein 10 (IP-10), a chemokine to attract CXCR3⁺ T helper 1-type CD4⁺ T cells, has not been investigated thoroughly in the pathogenesis of pancreatitis. B6 mice were inoculated intraperitoneally with LP-BM5 and then injected every week with either an antibody against IP-10 or a control antibody. Eight weeks after infection, we analyzed the effect of IP-10 neutralization. Anti-IP-10 antibody treatment did not change the generalized lymphadenopathy and hepatosplenomegaly of mice with MAIDS. The treatment significantly reduced the number of IP-10- and CXCR3-positive cells in the mesenteric lymph nodes (mLNs) but not the phenotypes and gross numbers of cells. In contrast, IP-10 neutralization reduced the number of mononuclear cells infiltrating into the pancreas. Anti-IP-10 antibody treatment did not change the numbers of IFN-⁺ and IL10⁺ cells in the mLN but significantly reduced their numbers, especially IFN-⁺ and IL-10⁺ CD4⁺ T cells and IFN-⁺ Mac-1⁺ cells, in the pancreas. IP-10 neutralization ameliorated the pancreatic lesions of mice with MAIDS probably by blocking the cellular infiltration of CD4⁺ T cells and IFN-⁺ Mac-1⁺ cells into the pancreas at least at 8 wk after infection, suggesting that IP-10 and these cells might play a key role in the development of chronic autoimmune pancreatitis.

autoimmune pancreatitis; Sjögren's syndrome; murine acquired immodeficiency syndrome; chemokines; interferon--inducible protein 10