IWASAKI Masayuki
   Department   Research Institutes and Facilities, Research Institutes and Facilities
   Position   Assistant Professor
Article types Original article
Language English
Peer review Peer reviewed
Title IFN-alpha acts on T-cell receptor-triggered human peripheral leukocytes to up-regulate CCR5 expression on CD4+ and CD8+ T cells.
Journal Formal name：Journal of clinical immunology
Abbreviation：J Clin Immunol
ISSN code：02719142/02719142
Domestic / ForeginForegin
Volume, Issue, Page 21(6),pp.402-9
Author and coauthor Yang Y F, Tomura M, Iwasaki M, Ono S, Zou J P, Uno K, Shearer G M, Fujiwara H, Hamaoka T
Publication date 2001/11
Summary Interleukin-12 (IL-12) as well as IL-2 was recently shown to up-regulate CCR5 expression on T-cell receptor (TCR)-triggered human T cells. Because of the functional similarity between interferon-alpha (IFN-alpha) and IL-12, the present study investigated whether IFN-alpha also up-regulates T cell CCR5 expression. CCR5 was marginally detected on T cells from unstimulated human peripheral blood leukocytes (PBLs) and only slightly induced on PBL T cells following stimulation with anti-CD3 plus anti-CD28 monoclonal antibodies (mAbs). When anti-CD3/anti-CD28-triggered PBLs were exposed to IFN-alpha, T cells expressed high levels of CCR5. The levels of CCR5 expression were comparable to those induced by IL-12. However, when purified T cells instead of unfractionated PBL were stimulated with anti-CD3/CD28 and then exposed to IL-12 or IFN-alpha, CCR5 expression was induced by IL-12 but not by IFN-alpha. IFN-alpha was found to act on anti-CD3/anti-CD28-stimulated PBL to promote their IL-12 production. Moreover, addition of anti-IL-12 mAb to IFN-alpha-stimulated cultures of anti-CD3/CD28-pretreated PBL resulted in considerable inhibition of CCR5 expression. Together, these results indicate that IFN-alpha as well as IL-12 up-regulates CCR5 expression on TCR-triggered T cells and that IFN-alpha functions not by acting directly on T cells but via enhancing IL-12 production by PBL.
DOI 10.1023/a:1013173610032
PMID 11811785