The mRNA and protein expression of the α- and β-chains of IFN-γR were evaluated on a panel of human Th1 and Th2 clones. When cultured in IL-2-conditioned medium, both types of clones expressed mRNA for the α- and β-chains, and both chains were present in the cytoplasm. Membrane expression of the α-chain was higher on Th2 than on Th1, whereas the β-chain was poorly expressed on both types but increased following IL-2 withdrawal or PHA stimulation. In addition, both types of clones overexpressed MHC class I glycoproteins following IFN-γR triggering by exogenous IFN-γ, although the kinetics was slower in Th1, and this exposure induced mRNA for IRF-1. When their TCR was triggered in the absence of ARC, Th1 only underwent apoptosis. This activation-induced apoptosis was prevented by blocking of the α-chain or by IFN-γ neutralization. Addition of IFN-γ triggered the apoptosis of Th2 clones. Apoptosis of both types of clones was mediated by autocrine or exogenous IFN-γ through the up-regulation of Fas-L expression, since anti-IFN-γRα mAb inhibited its expression on Th1 and exogenous IFN-γ increased its expression on Th2. These results indicate that activated human Th1 and Th2 lymphocytes express IFN-γR α- and β-chains and are both sensitive to signals provided by IFN-γ. Data also suggest that IFN-γ is critical for switching off their responses.
|Number of pages||8|
|Journal||Journal of Immunology|
|Publication status||Published - 1997|
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