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In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
Published on: October 15, 2013
In vitro protective and enhancing effects of interferons from several species on human lymphotoxin-induced target
In a previous study it was reported that human alpha-interferons (IFN) caused a significant enhancement of human lymphotoxin (LT)-induced in vitro killing of human target cells. This synergistic effect was dose dependent and was demonstrable on normal and tumor cell targets. The effects of IFNs from human and several animal species on human LT-induced cell killing of human, mouse, and rabbit target cells are examined. In addition to enhancement of IFN, a new finding was made showing protective effects of IFN on human LT activity. IFN-induced enhancement or protection depended on the particular IFN:target cell combination, with the highest degree of enhancement being observed in the homologous human combination. In this latter case, IFN-induced enhancement was blocked by antiserum to IFN. While a role for other soluble factors cannot be ruled out, the results suggest that, in the homologous human system, enhancement of LT activity was mediated by IFN. These results are discussed in relationship to previously observed enhancing and protective effects of IFN in natural killer cell systems.
In a previous study it was reported that human alpha-interferons (IFN) caused a significant enhancement of human lymphotoxin (LT)-induced in vitro killing of human target cells. This synergistic effect was dose dependent and was demonstrable on normal and tumor cell targets. The effects of IFNs from human and several animal species on human LT-induced cell killing of human, mouse, and rabbit target cells are examined. In addition to enhancement of IFN, a new finding was made showing protective effects of IFN on human LT activity. IFN-induced enhancement or protection depended on the particular IFN:target cell combination, with the highest degree of enhancement being observed in the homologous human combination. In this latter case, IFN-induced enhancement was blocked by antiserum to IFN. While a role for other soluble factors cannot be ruled out, the results suggest that, in the homologous human system, enhancement of LT activity was mediated by IFN. These results are discussed in relationship to previously observed enhancing and protective effects of IFN in natural killer cell systems.
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