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In this paper, the dynamics of stochastic human T‐cell leukemia virus type I (HTLV‐I) infection model with cytotoxic T lymphocyte (CTL) immune response is investigated. First, we show that the stochastic model exists as a unique positive global solution originating from the positive initial value. Second, we demonstrate that the stochastic model is stochastically permanent and stochastically ultimately bounded for any positive initial value. Third, we establish sufficient conditions for the existence of ergodic stationary distribution of the stochastic model. Fourth, the threshold R0∗ between extinction and persistence of the virus is obtained. Finally, numerical simulations are carried out to illustrate the theoretical results. [ABSTRACT FROM AUTHOR]

Tumour necrosis factor α (TNFα) inhibitors are widely used successfully as immunomodulatory agents in various autoimmune diseases. They primarily target the direct pro-inflammatory effect of TNFα. They have also been found to be critical for T-cell viability and activation. In this study we evaluated the effect of infliximab treatment under different in vitro stimulatory conditions of naive human cord blood T-cells and adult peripheral blood mononuclear cells (PBMC). PBMC and negatively selected cord blood naive human T-cells were stimulated with αCD3 with or without αCD28 co-stimulation. The role of in vitro infliximab treatment was evaluated in relation to transforming growth factor-β1 (TGF-β1) under the above different stimulatory conditions. Anti-TNFα treatment with infliximab significantly suppressed proliferation of adult and cord blood T-cells ( P < 0.013) during suboptimal stimulatory conditions. Infliximab prevented division of naive CD4+ and CD8+ T-cells and consequently also activation induced cell death, which was induced after three cell divisions. Interleukin (IL)-2 secretion was significantly decreased during infliximab treatment of suboptimally stimulated T-cells ( P < 0.05) while TGF-β1 levels were unchanged. Strikingly, the anti-proliferative effect of infliximab was overcome by the administration of anti-TGF-β1 or by the addition of exogenous IL-2. Interestingly, CD28 mediated co-stimulation restored the proliferative response in a dose–responsive manner during infliximab treatment. Finally, exogenous TNFα administration during suboptimal stimulation reduced the inhibitory effect of TGF-β1 upon proliferation ( P < 0.03). These results demonstrate that anti-TNFα treatment is primarily working upon T cells under low stimulatory conditions and probably through TGF-β1. [ABSTRACT FROM AUTHOR]

Studies the individuals infected with human T-cell lymphotropic virus type I (HTLV-I) in Brazil. Variety of T-cell epitopes that are recognized in the context of specific classes I and II human leucocyte antigen (HLA) molecules expressed by HTLV-I infected-T-cells; Determination of HLA-A, -B and -DR specificities by polymerase chain reaction with sequence-specific primers; Association of HLA-DR8 with adult T-cell leukemia/lymphoma.

The article focuses on human T cell lymphotropic virus-I (HTLV-I) infection and adult T cell leukemia. HTLV-I, the first discovered, is a C type retrovirus and a member of the group of transforming retroviruses. Cutaneous lesions are pleomorphic and resemble those of cutaneous T cell lymphoma, mycosis fungoides (MF) and are characterized by papules, nodules, and plaques but unlike MF they spread rapidly in the skin and disseminate to regional and central lymph nodes and to viscera. Adult T cell leukemia-lymphoma responds to combination chemotherapy but, remissions are usually short-lived and patients die within one year or two from infection or from their disease.