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Inhibition of IL-2 production by Nil-2-a in murine T cells

TitleInhibition of IL-2 production by Nil-2-a in murine T cells
Publication TypeArticolo su Rivista peer-reviewed
Year of Publication1998
AuthorsPucci, S., Doria G., Barile S., Pioli Claudio, and Frasca D.
JournalInternational Immunology
Volume10
Pagination1435-1440
ISSN09538178
KeywordsAge Factors, Aging, animal cell, Animals, article, CD4 antigen, CD4-Positive T-Lymphocytes, cycloheximide, Female, Genetic, Inbred C57BL, interleukin 2, Interleukin-2, lymphocyte activation, Messenger, messenger RNA, Mice, mouse, nonhuman, priority journal, RNA, T lymphocyte, T-Lymphocytes, Time Factors, Transcription, transcription regulation, zinc finger protein, Zinc Fingers
Abstract

The loss of IL-2 production is the main defect accounting for age-related immunodeficiencies. We have investigated the molecular mechanisms involved in the decrease of IL-2 production in CD4+ T cells from aging mice. Our results demonstrate that the stability of IL-2 mRNA increases in T cells from young mice, whereas it declines in T cells from old mice with the time of stimulation, suggesting the existence of different mechanisms of post-transcriptional regulation in young and old mice. We found that the IL-2 mRNA level in T cells from young but not from old mice increased up to 6- to 10-fold by addition of cycloheximide (CHX) while the stability of IL-2 mRNA is not affected. We then looked for IL-2 inducible inhibitory factors in T cells from young and old mice and demonstrated the presence of Nil-2-a, a zinc finger protein which negatively controls IL-2 gene transcription in human cells. This protein could be detected in T cells from both young and old mice, yet, in the presence of CHX, its binding activity was reduced by 75% in T cells from young but not from old mice. These findings show that Nil-2-a accounts for the negative control of IL-2 production in the mouse and explain the reduced IL-2 production in aging.

Notes

cited By 5

URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-0031660614&doi=10.1093%2fintimm%2f10.10.1435&partnerID=40&md5=9e2e61ebd5cc3a8a3223dcae5e7ff67d
DOI10.1093/intimm/10.10.1435
Citation KeyPucci19981435