Clarissa Rodrigues Nascimento
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Marco Antonio Lima
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Maria José de Andrada Serpa
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Otávio Espindola
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Ana Claudia Celestino Leite
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AbstractHuman T-cell lymphotropic virus type 1 (HTLV-1) is a causative agent of adult T-cell leukemia and HTLV-1–associated myelopathy/tropical spastic paraparesis. HTLV-1–associated myelopathy/tropical spastic paraparesis is a chronic inflammatory disease characterized by loss of motor movement in response to spinal marrow cell destruction by T lymphocytes. To perform their cellular function, T cells need to be activated by antigen-presenting cells, such as dendritic cells (DCs). The aim of this work was to analyze DC differentiation and activation from monocytes of HTLV-1–infected individuals. We demonstrated that monocytes from HTLV-1–infected patients who had been stimulated to differentiate had an impaired loss of CD14 expression, expressed low levels of CD1a, and maintained secretion of tumor necrosis factor-α compared with monocytes from noninfected donors. We further evaluated DC activation by tumor necrosis factor-α. We observed that in response to activation, DCs that were derived from noninfected donors had an increase in the percentage of CD83+, CD86+, and human leukocyte antigen-DR+ cells, whereas in DCs derived from HTLV-1–infected patients, the percentage of CD83+, CD86+, and human leukocyte antigen-DR+ cells remained similar to that of nonactivated cells. Moreover, these cells had an impaired capacity to stimulate allogeneic T lymphocytes. We demonstrated that DC maturation was altered in HTLV-1–infected patients, which could contribute to the development of HTLV-1–associated diseases.
A Combination of Human Leukocyte Antigen DQB1*02 and the Tumor Necrosis Factor α Promoter G308A Polymorphism Predisposes to an Insulin-Deficient Phenotype in Patients with Type 2 Diabetes