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Published on: June 19, 2014
Resistance to Fas-mediated apoptosis of human T-cell lines expressing human T-lymphotropic virus type-2 (HTLV-2) Tax
G Zehender1, S Varchetta, C De Maddalena
1Istituto di Malattie Infettive e Tropicali, Università degli Studi di Milano, 20100 Milano, Italy. zehender@mailserver.unimi.it
Abstract:
The susceptibility to Fas-mediated apoptosis was evaluated in seven T-cell lines (two infected with HTLV-2, one with HTLV-1, and four HTLV-free) as well as in Jurkat cells transfected with a Tax-2 expressing vector. Fas-mediated apoptosis was significantly reduced in the HTLV-1- and HTLV-2-infected lines in comparison with the HTLV-free lines regardless of the surface expression of Fas antigen (which was no different in the infected and uninfected cells). Fas-mediated apoptosis was also significantly inhibited in Jurkat cells transfected with the Tax-2 expressing vector without any modification in Fas expression. There was significantly more antiapoptotic Bcl-x(L) mRNA and protein in the transfected than in the untransfected Jurkat T cells. In conclusion, our results suggest that HTLV-2 is capable of inhibiting Fas-mediated apoptosis by means of a mechanism involving the tax-2 gene and probably the expression of bcl-x(L) messenger and protein.
Insights
Human T-cell leukemia virus type 2 (HTLV-2) inhibits Fas-mediated apoptosis, a programmed cell death pathway. This inhibition involves the tax-2 gene and likely upregulates Bcl-x(L) expression.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Fas-mediated apoptosis is a critical pathway for T-cell homeostasis and elimination of infected cells.
- Human T-cell leukemia viruses (HTLVs) are known to interfere with cellular processes, but the mechanisms are not fully elucidated.
- Understanding viral evasion strategies is crucial for developing therapeutic interventions.
Purpose of the Study:
- To investigate the effect of Human T-cell leukemia virus type 2 (HTLV-2) infection on Fas-mediated apoptosis in T-cells.
- To determine the role of the HTLV-2 Tax-2 protein in modulating apoptosis.
- To explore the involvement of Bcl-x(L) in HTLV-2-mediated resistance to apoptosis.
Main Methods:
- Evaluation of Fas-mediated apoptosis in HTLV-1, HTLV-2, and HTLV-free T-cell lines.
- Assessment of Fas antigen expression on T-cells.
- Analysis of apoptosis in Jurkat T-cells transfected with a Tax-2 expressing vector.
- Quantification of Bcl-x(L) mRNA and protein levels.
Main Results:
- HTLV-1 and HTLV-2 infected T-cell lines exhibited significantly reduced susceptibility to Fas-mediated apoptosis compared to HTLV-free lines.
- Fas expression levels were comparable between infected and uninfected T-cells, indicating apoptosis resistance is not due to altered Fas levels.
- Jurkat cells expressing the Tax-2 protein showed significant inhibition of Fas-mediated apoptosis.
- Transfected Jurkat cells displayed increased levels of antiapoptotic Bcl-x(L) mRNA and protein.
Conclusions:
- HTLV-2 infection confers resistance to Fas-mediated apoptosis in T-cells.
- The Tax-2 protein plays a key role in this antiapoptotic mechanism.
- Upregulation of Bcl-x(L) expression is likely involved in HTLV-2's ability to inhibit Fas-mediated apoptosis.
