Decay-accelerating factor (DAF) is a membrane protein that inhibits C3 convertase activity of autologous complement at the cell surface. We found that DAF+ cells and DAF- (DAFlow, if any) cells are clearly separated from each other among CD8-brightly positive (CD8bright) cells. Using three-color fluorescence flow cytometry, we found that whereas the CD8bright DAF- population express HLA-DR (class II major histocompatibility complex antigens, and an activated T cell marker), the CD8bright DAF+ population does not. Therefore, among the CD8bright T cells, DAF and HLA-DR are mutually exclusive. In addition, the CD8bright DAF+ population proliferates in the presence of recombinant interleukin 2 (rIL2) while the CD8bright DAF- population does not. After a 4-day cultivation of peripheral blood lymphocytes in the presence of rIL2, expression of HLA-DR increased in the CD8bright DAF- population and expression of IL 2Rp55 (alpha chain, the receptor for IL2, and a marker of T cell activation) occurred in the CD8bright DAF+ population. Furthermore, C3 deposition occurred in the CD8bright HLA-DR+ population which lacks DAF when lymphocytes, that had been cultured for 3 days in the presence of rIL2, were incubated with fresh autologous serum. This result suggests that the absence of DAF on CD8bright HLA-DR+ T cells might play a role in permitting complement reaction on the cells in vivo and may be related to the regulation of T cell activation.

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http://dx.doi.org/10.1002/eji.1830210810DOI Listing

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