Rescue of human T cells by interleukin-9 (IL-9) from IL-2 deprivation-induced apoptosis: correlation with alpha subunit expression of the IL-9 receptor.
Interleukin-9 (IL-9) is a Th2-derived cytokine that uses the gamma-chain of the IL-2 receptor for signaling. Therefore, the responsiveness of human Th1 and Th2 cell clones to IL-9 was measured by examining the ability of this cytokine to prevent apoptosis induced by IL-2 deprivation. A time course study demonstrated that both subsets of T cell clones underwent apoptosis with similar kinetics when deprived of IL-2 and that viability could be maintained by the addition of either IL-4 or IL-7. Interestingly, IL-9 prevented apoptosis in only 2 (Th2) of 14 clones tested. Analysis of IL-9R alpha subunit expression on 18 T cell clones revealed that IL-9 responsiveness was directly proportional to the expression of the high-affinity receptor. IL-9 responsiveness was also dependent on long-term culturing because neither freshly isolated nor 3-day phytohemagglutinin (PHA)- stimulated peripheral blood lymphocytes (PBL) expressed IL-9R alpha. In summary, the data showed that IL-9 can rescue only a small subset of Th2 cells from apoptosis induced by growth factor withdrawal and that expression of IL-9R alpha is required for the antiapoptotic signals mediated by this cytokine.[1]References
- Rescue of human T cells by interleukin-9 (IL-9) from IL-2 deprivation-induced apoptosis: correlation with alpha subunit expression of the IL-9 receptor. Perdow-Hickman, S., Salgame, P. J. Interferon Cytokine Res. (2000) [Pubmed]
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