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    Diabetes. 2007 Mar;56(3):809-17.

    CCL4 protects from type 1 diabetes by altering islet beta-cell-targeted inflammatory responses.

    Meagher C, Arreaza G, Peters A, Strathdee CA, Gilbert PA, Mi QS, Santamaria P, Dekaban GA, Delovitch TL.

    Laboratory of Autoimmune Diabetes, Robarts Research Institute, 100 Perth Drive, London, Ontario N6A 5K8, Canada.

    We previously reported that interleukin (IL)-4 treatment of nonobese diabetic (NOD) mice elevates intrapancreatic CCL4 expression and protects from type 1 diabetes. Here, we show that antibody neutralization of CCL4 abrogates the ability of T-cells from IL-4-treated NOD mice to transfer protection against type 1 diabetes. Intradermal delivery of CCL4 via a plasmid vector stabilized by incorporation of the Epstein-Barr virus EBNA1/oriP episomal maintenance replicon (pHERO8100-CCL4) to NOD mice beginning at later stages of disease progression protects against type 1 diabetes. This protection was associated with a Th2-like response in the spleen and pancreas; decreased recruitment of activated CD8(+) T-cells to islets, accompanied by diminished CCR5 expression on CD8(+) T-cells; and regulatory T-cell activity in the draining pancreatic lymph nodes. Thus, inflammatory responses that target islet beta-cells are suppressed by CCL4, which implicates the use of CCL4 therapeutically to prevent type 1 diabetes.

    PMID: 17327452 [PubMed - indexed for MEDLINE]

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