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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
Activation antigens on colonic T cells in inflammatory bowel disease: effects of IL-10
Activated T cells that express activation antigens are termed nonprofessional antigen-presenting cells (T-APCs). This study evaluates the ability of lamina propria lymphocytes (LPLs) in inflammatory bowel disease (IBD) to become T-APCs. LPLs were stained by two-colour immunofluorescence to determine the expression of activation antigens on T cells. Those from actively inflamed IBD mucosa expressed greater amounts of MHC class II (DR) and CD86 than did LPL T cells from disease controls or normal individuals. After culture in IL-2 with or without IL-10, the ability of the T-APCs from IBD colon to stimulate allogeneic peripheral blood T cell proliferation was measured. The T-APCs from IBD stimulated an allogeneic mixed lymphocyte reaction, particularly through their expression of DR and CD86, as demonstrated by antibody blocking. Normal LPLs acquired these properties only if repeatedly stimulated with allogeneic peripheral blood lymphocytes (PBLs) used as cell lines in the presence of IL-2. Addition of IL-10 reduced expression of activation antigens and the stimulatory ability of LPLs from either IBD patients or from these cell lines. In summary, LPLs from active IBD, but not from disease controls, express activation antigens that stimulate naïve T cells, a process that is reduced by IL-10. This may contribute to perpetuation of the inflammation.
Activated T cells that express activation antigens are termed nonprofessional antigen-presenting cells (T-APCs). This study evaluates the ability of lamina propria lymphocytes (LPLs) in inflammatory bowel disease (IBD) to become T-APCs. LPLs were stained by two-colour immunofluorescence to determine the expression of activation antigens on T cells. Those from actively inflamed IBD mucosa expressed greater amounts of MHC class II (DR) and CD86 than did LPL T cells from disease controls or normal individuals. After culture in IL-2 with or without IL-10, the ability of the T-APCs from IBD colon to stimulate allogeneic peripheral blood T cell proliferation was measured. The T-APCs from IBD stimulated an allogeneic mixed lymphocyte reaction, particularly through their expression of DR and CD86, as demonstrated by antibody blocking. Normal LPLs acquired these properties only if repeatedly stimulated with allogeneic peripheral blood lymphocytes (PBLs) used as cell lines in the presence of IL-2. Addition of IL-10 reduced expression of activation antigens and the stimulatory ability of LPLs from either IBD patients or from these cell lines. In summary, LPLs from active IBD, but not from disease controls, express activation antigens that stimulate naïve T cells, a process that is reduced by IL-10. This may contribute to perpetuation of the inflammation.
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