Abstract
A novel factor which augments the expression of major histocompatibility complex I (MHC augmenting factor or MHC-AF) antigens on tumor cell lines, has been isolated from the culture supernatants of human peripheral blood mononuclear cells activated by concanavalin-A. A mouse equivalent of this factor has also been isolated from the culture supernatants of mouse spleen cells activated by mitogens or in a mixed lymphocyte reaction. Mouse MHC-AF enhances the expression of class I MHC antigens on murine tumor cell lines (EL-4 and BW5147) but not on human tumor cell lines (K562 and HR-7). Human MHC-AF on the other hand enhances the MHC I expression on both human as well as murine cell lines. Interferon γ (IFN-γ), a cytokine also known to enhance the expression of MHC I antigens, acts in a highly species specific manner with mouse IFN-γ augmenting the MHC I on murine tumor cell lines and human IFN-γ augmenting the MHC I on human tumor cell lines only. These results indicate important differences in the cross species biological activities of MHC-AF and IFN-γ, and provide additional evidence for MHC-AF being distinct from IFN-γ.
Highlights
Major histocompatibility complex (MHC) antigens play a central role in interactions within immune cells and between cytotoxic lymphocytes and tumor cells (Zinkernagel and Doherty, 1979; Karre et al, 1986; Saxena, 1997)
K562 and HR7 human tumor cell lines were treated with mouse or human Interferon γ (IFN-γ) or with human or mouse MHC augmenting factor (MHC-AF) preparations for two days, and stained for expression of MHC class I antigens
Using the purification scheme standardized for rat MHC-AF, we have been able to partially purify a mouse MHC-AF from culture supernatants of mouse spleen cells activated in mixed lymphocyte reaction (Puri, 1995)
Summary
Major histocompatibility complex (MHC) antigens play a central role in interactions within immune cells and between cytotoxic lymphocytes and tumor cells (Zinkernagel and Doherty, 1979; Karre et al, 1986; Saxena, 1997). Many factors including interferon (Piontek et al, 1985; Wiebke et al.,1990), phorbol esters and sodium butyrate (Dokhelar et al, 1982,1984), are known to augment class I MHC expression on tumor cells. Work from our laboratory has described a putative novel cytokine termed MHC augmenting factor (MHC-AF), which enhances the class I MHC expression on tumor cells and renders them resistant to NK lysis (Saxena, 1987; Saxena et al, 1988, 1989, 1992, 1996; Puri, 1995; Raval et al, 1997). Our results indicate a major difference in species specificities between MHC–AF and IFN-γ
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