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Blood, 15 September 2008, Vol. 112, No. 6, pp. 2400-2410. Prepublished online as a Blood First Edition Paper on May 28, 2008; DOI 10.1182/blood-2008-02-138529. This Article Full Text (PDF) All Versions of this Article: blood-2008-02-138529v1 112/6/2400    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Enose-Akahata, Y. Articles by Jacobson, S. Search for Related Content PubMed PubMed Citation Articles by Enose-Akahata, Y. Articles by Jacobson, S. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 11, 2008 Accepted April 30, 2008 Retroviral-induced CTL degranulation mediated by IL-15 expression and infection of mononuclear phagocytes in patients with HTLV-I associated neurologic disease Yoshimi Enose-Akahata, Unsong Oh, Christian Grant, and Steven Jacobson* Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States * Corresponding author; email: jacobsons{at}ninds.nih.gov. CD8+ T cells contribute to central nervous system inflammation in HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). We analyzed CD8+ T cell dysfunction (degranulation and IFN- production) and have demonstrated that CD8+ T cells of patients with HAM/TSP spontaneously degranulate and expresse IFN- in ex vivo unstimulated short-term culture. HTLV-I asymptomatic carriers and healthy donors did not. Spontaneous degranulation was detected in Tax11-19/HLA-A*201 tetramer+ cells, but not in CMV pp65 tetramer+ cells. Interestingly, degranulation and IFN- production in CD8+ T cells was induced by co-culture with autologous CD14+ cells, but not CD4+ T cells, of patients with HAM/TSP, which correlated with proviral DNA load in CD14+ cells of infected patients. Moreover, the expression of IL-15, which induced degranulation and IFN- production in HTLV-I-infected patients, was enhanced on surface of CD14+ cells in patients with HAM/TSP. Blockade of MHC class I and IL-15 confirmed these results. Thus, CD8+ T cell dysregulation was mediated by both virus infection and enhanced IL-15 on CD14+ cells in patients with HAM/TSP. Despite low viral expression than in CD4+ T cells, HTLV-I-infected or activated CD14+ cells may be a heretofore important but under recognized reservoir particularly in patients with HTLV-I-associated neurological disease. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. R. M. Bangham HTLV-1 infection: role of CTL efficiency Blood, September 15, 2008; 112(6): 2176 - 2177. [Full Text] [PDF]

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