Low frequency of CD94/NKG2A+ T lymphocytes in patients with HTLV-1-associated myelopathy/tropical spastic paraparesis, but not in asymptomatic carriers

Saito, Mineki; Braud, Véronique M.; Goon, Peter; Hanon, Emmanuel; Taylor, Graham P.; Saito, Akiko; Eiraku, Nobutaka; Tanaka, Yuetsu; Usuku, Koichiro; Weber, Jonathan; Osame, Mitsuhiro; Bangham, Charles R. M.

doi:10.1182/blood-2002-09-2855

Cited by 37 publications

(19 citation statements)

References 44 publications

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“…The study by Saito et al (2003) and the earlier work by Yu et al (1991) and Fujihara et al (1991) suggested that the activity of the NK or NK-like cell response was associated with the presence or absence of HAM/TSP; the NK frequency and activity did not appear to correlate with proviral load. However, the recent data on lymphocyte gene expression indicated that high levels of expression of certain genes that encode proteins involved in NK cell-mediated lysis were associated with a low proviral load of HTLV-1.…”

Section: Natural Killer (Nk) Cell Response To Htlv-1mentioning

confidence: 85%

“…Using synthetic tetramers of HLA-E þ peptide to identify NK cells, Saito et al (2003) found a low frequency of HLA-E tetramerbinding cells in patients with HAM/TSP. Interestingly, as in the earlier studies Yu et al, 1991), this reduction in frequency was particularly notable in the CD3 þ cells, whereas there was no significant difference in the frequency of HLA-E tetramerbinding CD3…”

Section: Natural Killer (Nk) Cell Response To Htlv-1mentioning

confidence: 99%

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Cellular immune response to HTLV-1

2005

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There is strong evidence at the individual level and the population level that an efficient cytotoxic T lymphocyte (CTL) response to HTLV-1 limits the proviral load and the risk of associated inflammatory diseases such as HAM/TSP. This evidence comes from host population genetics, viral genetics, DNA expression microarrays and assays of lymphocyte function. However, until now there has been no satisfactory and rigorous means to define or to measure the efficiency of an antiviral CTL response. Recently, methods have been developed to quantify lymphocyte turnover rates in vivo and the efficiency of anti-HTLV-1 CTLs ex vivo. Data from these new techniques appear to substantiate the conclusion that variation between individual hosts in the rate at which a single CTL kills HTLV-1-infected lymphocytes is an important determinant, perhaps the decisive determinant, of the proviral load and the risk of HAM/ TSP. With these experimental data, it is becoming possible to refine, parameterize and test mathematical models of the immune control of HTLV-1, which are a necessary part of an understanding of this complex dynamic system.

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Section: Natural Killer (Nk) Cell Response To Htlv-1mentioning

confidence: 85%

Section: Natural Killer (Nk) Cell Response To Htlv-1mentioning

confidence: 99%

Cellular immune response to HTLV-1

2005

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“…For example, expression of CD94/NKG2A is lower in HAM/TSP patients, whereas an over-expression of NKG2D and NKG7 receptors has been found in HTLV-1-positive patients with low proviral load. Therefore, the participation of NK cells in disease outcome of HTLV-1-infected subjects remains a possibility [33,34].…”

Section: Discussionmentioning

confidence: 99%

Role of killer cell immunoglobulin-like receptor gene content and human leukocyte antigen–C group in susceptibility to human T-lymphotropic virus 1–associated myelopathy/tropical spastic paraparesis in Peru

et al. 2010

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“…The activity of NK cells is regulated by a balance between positive and negative signals from different activating and inhibitory NK receptors. CD94/NKG2 receptor family is expressed on CD8 + T cells and  T cells as well as NK cells, and is involved in the pathogenesis of HAM/TSP by modulating the activities of those cell populations (Saito et al 2003. In both HIV-1-and HTLV-1-infected individuals, the number and function of NK cell subsets are impaired (Fortis et al, 2005).…”

Section: Natural Killer Cells and Htlv-1mentioning

confidence: 99%