UNLABELLED: Dendritic cells (DC) were implicated as the mediators of primary stimulation of the immune response against donor antigen. Anti-lymphocytes globulin (ALG) and anti-thymocytes globulin (ATG) antibodies have been widely used as an immunosuppressive agent in the treatment and prevention of rejection after organ transplantation. In this study, we attempted to determine whether ATG and ALG are able to bind and interfere in human dendritic cell function. ALG and ATG bound to human DCs at least in part by recognising CD1a, MHC I, MHC II, CD11a, CD86, CD32, CD4, CD11b, CD29 and CD51/61. This binding, that was more relevant in mature DCs, induced complement-mediated lysis. ALG and ATG did not influence either the macropynocytosis of Lucifer Yellow (LY) or the receptor-mediated endocytosis of FITC-Dextran. In MLR assay, ATG and ALG were able to significantly inhibit T-cell proliferation by binding on T cell but not on dendritic cells. CONCLUSIONS: we demonstrate that ALG/ATG is able to interfere in the activation of T cells by dendritic cells in two different ways: by inhibiting the capacity of lymphocyte to proliferate after the DC stimulation and by inducing a complement-mediated lysis of DC. Copyright 2002 Elsevier Science B.V.
UNLABELLED: Dendritic cells (DC) were implicated as the mediators of primary stimulation of the immune response against donor antigen. Anti-lymphocytes globulin (ALG) and anti-thymocytes globulin (ATG) antibodies have been widely used as an immunosuppressive agent in the treatment and prevention of rejection after organ transplantation. In this study, we attempted to determine whether ATG and ALG are able to bind and interfere in human dendritic cell function. ALG and ATG bound to human DCs at least in part by recognising CD1a, MHC I, MHC II, CD11a, CD86, CD32, CD4, CD11b, CD29 and CD51/61. This binding, that was more relevant in mature DCs, induced complement-mediated lysis. ALG and ATG did not influence either the macropynocytosis of Lucifer Yellow (LY) or the receptor-mediated endocytosis of FITC-Dextran. In MLR assay, ATG and ALG were able to significantly inhibit T-cell proliferation by binding on T cell but not on dendritic cells. CONCLUSIONS: we demonstrate that ALG/ATG is able to interfere in the activation of T cells by dendritic cells in two different ways: by inhibiting the capacity of lymphocyte to proliferate after the DC stimulation and by inducing a complement-mediated lysis of DC. Copyright 2002 Elsevier Science B.V.
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