• Journal of Life Science
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• v.33 no.2
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• pp.149-157
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• 2023

Transforming growth factor-β (TGF-β) is a multifunctional cytokine that affects not only the survival and growth of cancer cells but also the activity of immune cells. Although it has been generally accepted that cancer cell-derived TGF-β could promote the survival and growth of early cancer cells and have immunosuppressive roles, it has been known that TGF-β has differential effects according to the type or stage of cancer cells. Therefore, it is hard to clearly define its role in cancer progression and immune responses. This study investigated the effects of TGF-β signaling on the expression of five NKG2D ligands and the NK cell-mediated anticancer immune response in the primary colon cancer cell line KM12C and its two metastatic cell lines, KM12SM and KM12L4A. At the surface protein level, exogenous TGF-β decreased the expression of MICA, MICB, ULBP1, and ULBP2, and galunisertib increased the expression of MICA, MIAB, ULBP1, ULBP2, and ULBP3 in KM12C. However, KM12SM and KM12L4A showed no significant changes in the expression of NKG2DLs after treatment with TGF-β or galunisertib. TGF-β signaling inhibition via galunisertib improved the NK cell-mediated anticancer immune response against KM12C but did not show a significant response to KM12SM and KM12L4A. Therefore, the suppression of TGF-β signaling could improve the NK cell-mediated anticancer immune response against KM12C. However, an increase in NKG2DLs expression and an enhanced NK cell-mediated cancer immune response is hard to expect due to the alteration of TGF-β signaling in KM12SM and KM12L4A.

• The Journal of the Korean Society for Microbiology
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• v.14 no.1
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• pp.79-87
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• 1979

The immunosuppressive activity of newcastle disease virus(NDV) and some possible role of interferon(C-IF) in viral suppression of immune response were evaluated by SRBC-induced delayed-type hypersensitivity(DTH), rosette formation in spleen cells, number of lymphocytes in peripheral blood, hemagglutinin and hemolysin response to SRBC in ICR mice sensitized with SRBC. When NDV was inoculated before or after sensitization of mouse with SRBC, virus caused a marked inhibition of DTH, and its depressive effect was dependent on the time of virus inoculation in relation to SRBC sensitization or challenge. Rosette formation of spleen cells was significantly reduced by NDV infection. The degree of the depression of rosette formation was more prominent in mice inoculated before sensitization than after sensitization and could be related to the amount of serum interferon induced by the virus. Humoral response to SRBC of virus infected mouse was significantly depressed when NDV was inoculated 24 or 48 hours before sensitization. However, there was no difference in the response when the virus was inoculated 9 hour before and at the same time of sensitization or even after that. Lymphocytes in peripheral blood of mice were markedly diminished in numbers when NDV was inoculated 48 and 24 hour before sensitization with SRBC, but they were slightly augmented when the virus was inoculated 9 hour before and at the same time of sensitization. When UV-inactivated or heat-inactivated NDV was injected to the mouse at the same time of sensitization with SRBC, DTH and rosette formation of spleen cells were slightly depressed. DTH and rosette formation in mice treated with crude-IF were generally depressed as com pared with those of control mice. These studies suggest that the NDV causes a significant depression of cell-mediated immunity, whereas the humoral immune response is not inhibited markedly, and that the depression of immune response by NDV infection may be caused by interferon produced by NDV and direct viral activity.