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The Influence of Tumour Necrosis Factor‐γ, Interleukin‐1β and Interferon‐γ on the Expression and Function of the Complement Regulatory Protein CD59 on the Human Colonic Adenocarcinoma Cell Line HT29
Author(s) -
BJØRGE L.,
JENSEN T. SKEIE,
ULVESTAD E.,
VEDELER C. A.,
MATRE R.
Publication year - 1995
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1995.tb03578.x
Subject(s) - cd59 , decay accelerating factor , biology , tumor necrosis factor alpha , cytokine , peripheral blood mononuclear cell , interferon gamma , cell culture , microbiology and biotechnology , immunology , cancer research , complement system , in vitro , immune system , biochemistry , genetics
CD59 is a 18–25kDa glycoprotein which, by inhibiting the formation of the membrane attack complex, protects homologous cells from complement mediated damage. We have described recently the expression and complement regulatory function of CD59 on colonic adenocarcinoma cells both in vivo and in vitro. In this study we have examined the influence of cytokines on the expression and complement regulatory function of CD59 on the colonic adenocarcinoma cell line HT29. CD59 expression on the HT29 cells was up–regulated after stimulation by mononuclear cells activated by mixed lymphocyte reaction and by culture supernatants from activated mononuclear cells. Similarly, a dose–dependent increase in CD59 expression was observed after stimulation with both tumour necrosis factor‐γ and interleukin‐1β. A dose–dependent increase in the level of CD59 expression was also seen using low concentrations of interferon‐γ (IFN‐γ), while CD59 expression on cells cultured with high IFN‐γ concentrations was comparable to non–stimulated cells. Cytokine treated cells were more resistant to lysis by homologous complement than non–stimulated cells, and the increase in CD59 expression was shown to be partially responsible for this. The present data strengthen the role of CD59 as a possible participant in tumour escape.