Search for: [Abstract = "e transferred with as 4x105 peripheral lymph node cells. Further, the effects of skin\-induced suppression was found to decline with time. However, neither mesenteric lymph node cells or thymocytes could transfer EC induced tolerance. Depletion experiments using anti\-TCRβ or anti\-TCRδ monoclonal antibodies \(mAb\) and complement revealed that EC induced suppressor cells belong to the population of TCRαβ\+ lymphocytes. To identify the phenotype of EC induced regulatory cells more precisely, total lymph node cells from mice EC tolerized with COLL II were depleted of either CD4 or CD8 T cells by treatment with mAb and complement prior to transfer into syngeneic DBA\/1 recipients. Protection was abrogated when either CD4 or CD8 T cells were depleted. Combining CD4\-depleted lymphocytes with CD8\-depleted lymphocytes, thereby reconstituting the populations of single\-positive cells, did not restore protection from disease, suggest that EC\-induced T regulatory cells co\-express both CD4 and CD8 coreceptors. In summary, these data suggest that EC immunization with COLL II induces a population of regulatory T cells with a TCRαβ\+ CD4\+ CD8\+ phenotype. Surprisingly, suppression was not specific to antigen, as EC immunization with any tested protein antigen \(COLL II, OVA or MBP\) prior to induction of CIA reduced disease severity. To determine the mechanism of EC induced suppression in CIA, the ex"]

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