منابع مشابه
High frequency of CD4+FoxP3+ cells in HTLV-1 infection: inverse correlation with HTLV-1–specific CTL response
Evidence from population genetics, gene expression microarrays, and assays of ex vivo T-cell function indicates that the cytotoxic T lymphocyte (CTL) response to human T-lymphotropic virus type 1 (HTLV-1) controls the level of HTLV-1 expression and the proviral load. The rate at which CTLs kill autologous HTLV-1-infected lymphocytes differs significantly among infected people, but the reasons f...
متن کاملThe avidity and lytic efficiency of the CTL response to HTLV-1.
In human T-lymphotropic virus type 1 (HTLV-1) infection, a high frequency of HTLV-1-specific CTLs can co-exist stably with a high proviral load and the proviral load is strongly correlated with the risk of HTLV-1-associated inflammatory diseases. These observations led to the hypothesis that HTLV-1 specific CTLs are ineffective in controlling HTLV-1 replication but contribute to the pathogenesi...
متن کاملPrevalence of HTLV-1 infection in Golestan Province, Iran
Abstract Background and objectives: Human T-Lymphocyte Virus-1 (HTLV- 1) is known as the etiologic factor of acute T-Lymphocytic Leukemia (ATL) and tropical spastic paralysis. (TSP). Endemic factors causing infection with Human T Lymphocyte Virus-1 (HTLV-1) is based on environmental, socio-economical and health behaviors of the individuals. This virus is well distributed in families with involv...
متن کاملInvestigation of the Relationship between HTLV-1 Infection and MMP-3 Gene Expression in HTLV-1 Positive Cardiac Patients
Background and Aims: Human T-lymphotropic virus type 1 (HTLV-1) is a member of retroviridae family that causes ATL and HAM/TSP. Many inflammatory diseases are associated with this virus, such as Sjögren's syndrome, Hashimoto's thyroiditis, Uveitis and also Atherosclerosis. HTLV-1 performs in long latency period and can activate the immune responses in coronary vessels. Activated immune sys...
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ژورنال
عنوان ژورنال: Blood
سال: 2008
ISSN: 0006-4971,1528-0020
DOI: 10.1182/blood-2008-06-163071