Abstract
BackgroundCD4+CD25high regulatory T (TReg) cells modulate antigen-specific T cell responses, and can suppress anti-viral immunity. In HTLV-1 infection, a selective decrease in the function of TReg cell mediated HTLV-1-tax inhibition of FOXP3 expression has been described. The purpose of this study was to assess the frequency and phenotype of TReg cells in HTLV-1 asymptomatic carriers and in HTLV-1-associated neurological disease (HAM/TSP) patients, and to correlate with measures of T cell activation.ResultsWe were able to confirm that HTLV-I drives activation, spontaneous IFNγ production, and proliferation of CD4+ T cells. We also observed a significantly lower proportion of CTLA-4+ TReg cells (CD4+CD25high T cells) in subjects with HAM/TSP patients compared to healthy controls. Ki-67 expression was negatively correlated to the frequency of CTLA-4+ TReg cells in HAM/TSP only, although Ki-67 expression was inversely correlated with the percentage of CD127low TReg cells in healthy control subjects. Finally, the proportion of CD127low TReg cells correlated inversely with HTLV-1 proviral load.ConclusionTaken together, the results suggest that TReg cells may be subverted in HAM/TSP patients, which could explain the marked cellular activation, spontaneous cytokine production, and proliferation of CD4+ T cells, in particular those expressing the CD25highCD127low phenotype. TReg cells represent a potential target for therapeutic intervention for patients with HTLV-1-related neurological diseases.
Highlights
CD4+CD25high regulatory T (TReg) cells modulate antigen-specific T cell responses, and can suppress anti-viral immunity
In this study we addressed the relationship between TReg cells, T cell activation, and HTLV-1 infected patients who were clinically asymptomatic (HTLV)-1 proviral load
Infection with HTLV-1 was associated with higher spontaneous IFNγ release by CD4+ T cells, but only in HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) there was a marked increase in T cell proliferation
Summary
CD4+CD25high regulatory T (TReg) cells modulate antigen-specific T cell responses, and can suppress anti-viral immunity. It has been estimated that the prevalence of HTLV-1 infection in South America ranges from 2 to 5% [4], with an estimated 1–2 million infected people in Brazil [5]. Tax has the ability of interfering in the expression of several transcription factors and proto-oncogenes, as well as in the nucleic acid repair and apoptosis [14,15,16,17]. These effects combined seem to play a key role in the potential of HTLV-1 to induce cellular transformation and, trigger the development of ATLL
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