Interleukin-7 rescues human activated T lymphocytes from apoptosis induced by glucocorticoesteroids and regulates bcl-2 and CD25 expression

• Published in: Human immunology 1995-07, Vol.43 (3), p.181-189
• Main Authors: Hernández-Caselles, Trinidad, Mertíndez-Esparza, María, Sancho, David, Rubio, Gonzalo, Aparicio, Pedro
• Format: Article
• Language: English
• Subjects: Apoptosis; Dexamethasone - adverse effects; Gene Expression Regulation; Glucocorticoids - adverse effects; Humans; Interleukin-2 - immunology; Interleukin-4 - immunology; Interleukin-7 - genetics; Interleukin-7 - pharmacology; Proto-Oncogene Proteins - biosynthesis; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins c-bcl-2; Receptors, Interleukin-2 - biosynthesis; Receptors, Interleukin-2 - genetics; Recombinant Proteins - immunology; T-Lymphocytes - immunology
• ISSN: 0198-8859; 1879-1166
• DOI: 10.1016/0198-8859(94)00168-P

We studied the ability of several interleukins to inhibit the cellular death of IL-2-dependent human T cells deprived of IL-2 testing viability, DNA integrity, and expression of bcl-2 gene product. Our in vitro results showed that the addition of IL-7, and in a far less efficient manner IL-4, augmented the viability of IL-2-dependent T-cell clones of different origin, specificity, and phenotype. Furthermore, IL-7 reduced the percentage of apoptotic T cells inhibiting DNA fragmentation. In addition, IL-7 but not IL-4 was consistently able to suppress the cell death of IL-2-dependent T cells triggered by DEX, a synthetic GC. The suppression of T-cell death triggered by IL-7 was not affected by the addition of anti-IL-2 antibody. Interestingly, IL-7 inhibited the downregulation of bcl-2 gene product expression that appeared on TCCs after IL-2 withdrawal and also shared with IL-2 the ability to induce the upregulation of CD25 antigen on activated T lymphocytes in the presence of DEX. These experiments establish a novel role for IL-7 in regulating viability and GC-induced apoptosis on activated human T cells and suggest that the maintenance of bcl-2 levels is a general mechanism by which interleukins preserve activated T cells from undergoing apoptosis.