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Kozako, T. et al.

Reduced Frequency, Diversity, and Function of Human T Cell Leukemia Virus Type 1-Specific CD8+ T Cell in Adult T Cell Leukemia Patients.

Human T cell lymphotropic virus type 1 (HTLV-1)-specific CTL are thought to be immune effectors that reduce the risk of adult T cell leukemia (ATL). However, in vivo conditions of anti-HTLV-1 CTL before and after ATL development have yet to be determined. To characterize anti-HTLV-1 CTL in asymptomatic HTLV-1 carriers ( AC) and ATL patients, we analyzed the frequency and diversity of HTLV-1-specific CD8(+) T cells in PBMC of 35 AC and 32 ATL patients using 16 distinct epitopes of HTLV-1 Tax or Env/HLA tetramers along with intracellular cytolytic effector molecules (IFN-gamma, perforin, and granzyme B). Overall frequency of subjects possessing Tax-specific CD8(+) T cells was significantly lower in ATL than AC (53 vs 90%; p = 0.001), whereas the difference in Env-specific CD8(+) T cells was not statistically significant. AC possessed Tax(11-19)/HLA-A*0201-specific tetramer(+) cells by 90% and Tax(301-309)/HLA-A*2402-specific tetramer(+) cells by 92%. Some AC recognized more than one epitope. In contrast, ATL recognized only Tax(11-19) with HLA-A*0201 and Tax(301-309) with HLA-A*2402 at frequencies of 30 and 55%. There were also significant differences in percentage of cells binding Tax(11-19)/HLA-A*0201 and Tax(301-309)/HLA-A*2402 tetramers between AC and ATL. Anti-HTLV-1 Tax CD8(+) T cells in AC and ATL produced IFN-gamma in response to Tax. In contrast, perforin and granzyme B expression in anti-HTLV-1 CD8(+) T cells of ATL was significant lower than that of AC. Frequency of Tax-specific CD8(+) T cells in AC was related to proviral load in HLA-A*0201. These results suggest that decreased frequency, diversity, and function of anti-HTLV-1 Tax CD8(+) T cell clones may be one of the risks of ATL development.[1]

References

Reduced Frequency, Diversity, and Function of Human T Cell Leukemia Virus Type 1-Specific CD8+ T Cell in Adult T Cell Leukemia Patients. Kozako, T., Arima, N., Toji, S., Masamoto, I., Akimoto, M., Hamada, H., Che, X.F., Fujiwara, H., Matsushita, K., Tokunaga, M., Haraguchi, K., Uozumi, K., Suzuki, S., Takezaki, T., Sonoda, S. J. Immunol. (2006) [Pubmed]

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