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      Cutting edge: cure of colitis by CD4+CD25+ regulatory T cells.

      The Journal of Immunology Author Choice

      Adoptive Transfer, methods, Animals, Antigens, CD11c, biosynthesis, CD4-Positive T-Lymphocytes, cytology, immunology, metabolism, transplantation, Cell Communication, Cell Division, Cell Movement, Colitis, pathology, therapy, Colon, Lymph Nodes, Mesentery, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, SCID, Receptors, Interleukin-2, T-Lymphocyte Subsets, Wasting Syndrome

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          CD4(+)CD25(+) regulatory T cells have been shown to prevent T cell-mediated immune pathology; however, their ability to ameliorate established inflammation has not been tested. Using the CD4(+)CD45RB(high) T cell transfer model of inflammatory bowel disease, we show that CD4(+)CD25(+) but not CD4(+)CD25(-)CD45RB(low) T cells are able to cure intestinal inflammation. Transfer of CD4(+)CD25(+) T cells into mice with colitis led to resolution of the lamina propria infiltrate in the intestine and reappearance of normal intestinal architecture. CD4(+)CD25(+) T cells were found to proliferate in the mesenteric lymph nodes and inflamed colon. They were located between clusters of CD11c(+) cells and pathogenic T cells and found to be in contact with both cell types. These studies suggest that manipulation of CD4(+)CD25(+) T cells may be beneficial in the treatment of chronic inflammatory diseases.

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