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Kubota R, Nagai M, Kawanishi T, et al. Increased HTLV type 1 tax specific CD8+ cells in HTLV type 1-asociated myelopathy/tropical spastic paraparesis: correlation with HTLV type 1 proviral load. AIDS Res Hum Retroviruses. 2000;16(16):1705-9doi: 10.1089/08892220050193182.
Kubota, R., Nagai, M., Kawanishi, T., Osame, M., & Jacobson, S. (2000). Increased HTLV type 1 tax specific CD8+ cells in HTLV type 1-asociated myelopathy/tropical spastic paraparesis: correlation with HTLV type 1 proviral load. AIDS research and human retroviruses, 16(16), 1705-9. https://doi.org/10.1089/08892220050193182
Kubota, R, et al. "Increased HTLV type 1 tax specific CD8+ cells in HTLV type 1-asociated myelopathy/tropical spastic paraparesis: correlation with HTLV type 1 proviral load." AIDS research and human retroviruses vol. 16,16 (2000): 1705-9. doi: https://doi.org/10.1089/08892220050193182
Kubota R, Nagai M, Kawanishi T, Osame M, Jacobson S. Increased HTLV type 1 tax specific CD8+ cells in HTLV type 1-asociated myelopathy/tropical spastic paraparesis: correlation with HTLV type 1 proviral load. AIDS Res Hum Retroviruses. 2000 Nov 01;16(16):1705-9. doi: 10.1089/08892220050193182. PMID: 11080814.
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AIDS Res Hum Retroviruses. 2000 Nov 01;16(16):1705-9. doi: 10.1089/08892220050193182.

Increased HTLV type 1 tax specific CD8+ cells in HTLV type 1-asociated myelopathy/tropical spastic paraparesis: correlation with HTLV type 1 proviral load.

AIDS research and human retroviruses

R Kubota, M Nagai, T Kawanishi, M Osame, S Jacobson

Affiliations

  1. Viral Immunology Section, NIB, NINDS, NIH, Bethesda, Maryland 20892, USA.

PMID: 11080814 DOI: 10.1089/08892220050193182

Abstract

Less than 1% of individuals infected with the human T lymphotropic virus type 1 (HTLV-1) develop an inflammatory neurological disorder, termed HTLV-1-associated myelopathy/tropical spastic (HAM/TSP), while the vast majority of those infected remain asymptomatic HTLV-1 carriers (ACs). The fundamental viroimmunological differences between these groups are not well understood. To address this issue, we have investigated HTLV-1-specific T cell responses and measured the proviral load in these groups. Frequencies of HTLV-1-specific CD8(+) cells were demonstrated to be significantly higher in HAM/TSP patients than in ACs by using intracellular cytokine staining and soluble divalent HLA-A2/Ig fusion protein loaded with HTLV-1 Tax 11-19 peptide. It is consistent with the observed increase in HTLV-1-specific cytotoxic T lymphocytes in HAM/TSP patients. These CD8(+) cells produced interferon (IFN)-gamma in recognition of HTLV-1 antigens bound to HLAs on the infected CD4(+) cells. Using phenotypic markers indicative for T cell differentiation, memory and/or effector HTLV-1 Tax-specific CD8(+) cells were found to be increased in HLA-A2 HAM/TSP patients. HTLV-1 proviral load was elevated in HAM/TSP patients when compared to ACs. In addition, the proviral load in HAM/TSP patients correlated with the frequency of HTLV-1-specific IFN-gamma(+)CD8(+) cells or Tax-HLA-A2/Ig(+)CD8(+) cells, especially with the effector cells. In contrast, the proviral load inversely correlated with memory cells. These results suggest that HTLV-1 antigens may continuously stimulate HTLV-1-specific CD8(+) cells and differentiate them from memory cells into effector cells in vivo. These differentiated HTLV-1-specific CD8(+) cells may play a role in the pathogenesis of HAM/TSP.

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